KDIGO 2024 Clinical Practice Guideline for the Evaluation and

VOLUME 105 | ISSUE 4S | APRIL 2024

www.kidney-international.org

KDIGO 2024 Clinical Practice Guideline for the

Evaluation and Management of Chronic Kidney Disease

SUPPLEMENT TO

KDIGO 2024 CLINICAL PRACTICE GUIDELINE

FOR THE EVALUATION AND MANAGEMENT

OF CHRONIC KIDNEY DISEASE

Kidney International (2024) 105 (Suppl 4S), S117–S314 S117

KDIGO 2024 Clinical Practice Guideline for the Evaluation and

Management of Chronic Kidney Disease

S118 Tables, ﬁgures, and supplementary material

S124 KDIGO Executive Committee

S125 Reference keys

S126 CKD nomenclature

S127 Conversion factors

S128 Abbreviations and acronyms

S129 Notice

S130 Foreword

S131 Work Group membership

S133 Abstract

S134 Patient foreword

S135 Introduction, qualifying statements, and key concepts

S141 Special considerations

S144 Summary of relative and absolute risks relevant to CKD from meta-analysis of

large multinational population studies in the CKD Prognosis Consortium

(CKD-PC)

S149 Summary of recommendation statements and practice points

S169 Chapter 1: Evaluation of CKD

S196 Chapter 2: Risk assessment in people with CKD

S205 Chapter 3: Delaying CKD progression and managing its complications

S246 Chapter 4: Medication management and drug stewardship in CKD

S255 Chapter 5: Optimal models of care

S270 Chapter 6: Research recommendations

S274 Methods for guideline development

S283 Biographic and disclosure information

S294 Acknowledgments

S295 References

This article is published as part of a supplement sponsored by Kidney Disease: Improving Global Outcomes (KDIGO). The

opinions or views expressed in this supplement are those of the authors and do not necessarily reﬂect the opinions or rec-

ommendations of the International Society of Nephrology or Elsevier. Dosages, indications, and methods of use for products

that are referred to in the supplement by the authors may reﬂect their clinical experience or may be derived from the pro-

fessional literature or other clinical sources. Because of the differences between in vitro and in vivo systems and between

laboratory animal models and clinical data in humans, in vitro and animal data do not necessarily correlate with clinical results.

contents www.kidney-international.org

VOL 105 | ISSUE 4S | APRIL 2024

S118 Kidney International (2024) 105 (Suppl 4S), S117–S314

TABLES

S137 Table 1. Criteria for chronic kidney disease

S137 Table 2. GFR categories in CKD

S137 Table 3. Albuminuria categories in chronic kidney disease (CKD)

S169 Table 4. Use of GFR and albuminuria

S171 Table 5. Risk factors for CKD

S174 Table 6. Guidance for selection of additional tests for evaluation of cause

S178 Table 7. Description of initial and supportive tests for evaluation of GFR

S179 Table 8. Indications for use of cystatin C

S180 Table 9. Comparison of estimated GFR and measured GFR

S181 Table 10. Indications for measured GFR

S184 Table 11. Implementation standards to ensure accuracy and reliability of GFR assessments using creatinine and

cystatin C

S184 Table 12. Reported examples of substances that may cause analytical interferences in creatinine assays

S187 Table 13. Criteria for a validated GFR estimating equation

S189 Table 14. Validated GFR estimating equations

S190 Table 15. Criteria for equation comparison for comparison of candidate equations to another (i.e., how to

determine validity)

S191 Table 16. Factors causing biological variation in urine albumin or urine protein

S193 Table 17. Implementation standards to ensure accuracy and reliability of urine samples

S198 Table 18. Impact of albuminuria/proteinuria on CKD progression in pediatrics

S199 Table 19. Externally validated risk equations for predicting kidney failure in the general (CKD G3–G5)

population

S203 Table 20. Externally validated risk equations for predicting a 40% decline in GFR

S209 Table 21. Impact of plant-based foods in people with CKD

S212 Table 22. Age-based sodium intake recommendations

S222 Table 23. Variation of laboratory values in a large population database by age group, sex, and eGFR; bicarbonate,

mmol/l, mean (SD), n [ 3,990,898

S223 Table 24. Variation of laboratory values in a large population database by age group, sex, and eGFR; potassium,

mmol/l, mean (SD), n [ 4,278,600

S225 Table 25. Factors and mechanisms that impact on potassium measurements

S226 Table 26. Medications associated with increased risk of hyperkalemia

S227 Table 27. A comparison of potassium exchange agents

S227 Table 28. Suggested action in the event of moderate and severe hyperkalemia

S229 Table 29. Variation of laboratory values in a large population database by age group, sex, and eGFR; hemoglobin,

g/dl, mean (SD), n [3,561,622

S233 Table 30. Randomized controlled trials in the treatment of asymptomatic hyperuricemia in people with CKD

S247 Table 31. Key examples of common medications with documented nephrotoxicity and, where available, selected

non-nephrotoxic alternatives

S252 Table 32. Medications that should be considered for temporary discontinuation before elective surgeries and

potential perioperative adverse events associated with their continued use

S253 Table 33. Potential risk factors for contrast-associated acute kidney injury

S256 Table 34. Beneﬁts and consequences of early versus late referral

S257 Table 35. Factors associated with late referral for kidney replacement therapy planning

S257 Table 36. Outcomes examined in a systematic review by Smart et al.

S258 Table 37. Recommended patient-reported outcome measurement tools for use in people with CKD

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S259 Table 38. Management strategies for common symptoms in CKD

S261 Table 39. List of validated assessment tools for malnutrition

S262 Table 40. Key features of existing CKD care models

S266 Table 41. Indications for the initiation of dialysis

S267 Table 42. Studies examining the timing of dialysis in people with CKD

S268 Table 43. People with kidney failure who receive comprehensive conservative care

S275 Table 44. Clinical questions and systematic review topics in PICOS format

S280 Table 45. Classiﬁcation for certainty of evidence

S280 Table 46. GRADE system for grading the certainty of evidence

S281 Table 47. KDIGO nomenclature and description for grading recommendations

S281 Table 48. Determinants of the strength of recommendation

FIGURES

S136 Figure 1. Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by

creatinine and cystatin C (eGFRcr-cys) and albumin-to-creatinine ratio (ACR) categories an d risks for

10 common complications by age in multivariable-adjusted analyses

S138 Figure 2. Age-standardized chronic kidney disease disability-adju sted life-year (DALY) rates for each location by

sociodemographic index, both sexes combined, 2019

S139 Figure 3. Screening algorithm for diagnosis and staging of chronic kidney disease (CKD) in adults

S141 Figure 4. Special considerations for chronic kidney disease (CKD) care across the lifespan

S145 Figure 5. Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by

creatinine (eGFRcr) and albumin-to-creatinine ratio (ACR) categories and risks for 10 common

complications in multivariable-adjusted analyses

S146 Figure 6. Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by

creatinine and cystatin C (eGFRcr-cys) and albumin-to-creatinine ratio categories and risks for 10

common complications in multivariable-adjusted analyses

S147 Figure 7. Hazard ratios for adverse outcomes using the continuous model of estimated glomerular ﬁltration rate

(eGFR), comparison of the shape of associations between creatinine-based eGFR (eGFRcr) and

creatinine and cystatin C–based eGFR (eGFRcr-cys) in the population with cystatin C (eGFRcr-cys

population)

S173 Figure 8. Evaluation of cause of chronic kidney disease (CKD)

S174 Figure 9. Actionable genes in kidney disease

S175 Figure 10. Proposed organization for implementing genetics in nephrology

S177 Figure 11. Approach to glomerular ﬁltration rate (GFR) evaluation using initial and supportive tests

S182 Figure 12. Sources and magnitude of error around measured glomerular ﬁltration rate (mGFR) and estimated GFR

(eGFR)

S197 Figure 13. Frequency of monitoring glomerular ﬁltration rate (GFR) and albuminuria in people with chronic

kidney disease (CKD)

S199 Figure 14. (a) Predicted risk of kidney failure and (b) ‡40% decline in estimated glomerular ﬁltration rate (eGFR)

by chronic kidney disease (CKD) eGFR (G1–G5) and albumin-to-creatinine ratio (ACR) (A1–A3)

categories in Optum Labs Data Warehouse

S201 Figure 15. Transition from an estimated glomerular ﬁltration rate (eGFR)-based to a risk-based approach to

chronic kidney disease care

S202 Figure 16. Comparison of risk of chronic kidney disease (CKD) progression (5-year probability of estimated

glomerular ﬁltration rate [eGFR] <60 ml/min per 1.73 m

) versus kidney failure in adults with CKD G1–

G2 calculated from the risk equation available at https://www.ckdpc.org/risk-models.html

S205 Figure 17. Chronic kidney disease (CKD) treatment and risk modiﬁcation

S206 Figure 18. Holistic approach to chronic kidney disease (CKD) treatment and risk modiﬁcation

S208 Figure 19. Protein guideline for adults with chronic kidney disease not treated with dialysis

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Kidney International (2024) 105 (Suppl 4S), S117–S314

S209 Figure 20. Average protein content of foods in grams

S214 Figure 21. Algorithm for monitoring of potassium and estimated glomerular ﬁltration rate (eGFR) after the initiation

of renin-angiotensin system inhibitors

S215 Figure 22. Effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) with kidney disease outcomes by diabetes

status

S216 Figure 23. Effects of sodium-glucose cotransporter-2 (SGLT2) inhibition versus placebo on cardiovascular and

mortality outcomes by diabetes status and trial population

S217 Figure 24. Effects of sodium-glucose cotransporter-2 (SGLT2) inhibition versus placebo on kidney failure (chronic

kidney disease [CKD] trials)

S219 Figure 25. Effects of empagliﬂozin versus placebo on annual rate of change in estimated glomerular ﬁltration rate

(GFR) by key subgroups in the Study of Heart and Kidney Protection With Empagliﬂozin (EMPA-

KIDNEY)

S220 Figure 26. Serum potassium monitoring during treatment with a nonsteroidal mineralocorticoid receptor

antagonist (MRA) (ﬁnerenone)

S221 Figure 27. Effect of ﬁnerenone versus placebo on kidney and cardiovascular outcomes in pooled analyses from the

Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease (FIDELIO-

DKD) and Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease

(FIGARO-DKD trials)

S222 Figure 28. Association between estimated glomerular ﬁltration rate (eGFR) with serum bicarbonate

concentration in general population and h igh-risk cohorts from the Chronic Kidney Disease

Prognosis Consortium, by level of albuminuria (A1–A3)

S224 Figure 29. Distribution of blood potassium in general population and high-risk cohorts from the Chronic Kidney

Disease Prognosis Consortium, by estimated glomerular ﬁltration rate (eGFR)

S224 Figure 30. Meta-analyzed adjusted prevalence of hyperkalemia (25th and 75th percentile cohort) in general

population and high-risk cohorts from the Chronic Kidney Disease Prognosis Consortium, by diabetes

status

S225 Figure 31. Serum potassium concentration and confounder-adjusted risk of death by presence or absence of

diabetes, heart failure (HF), or chronic kidney disease (CKD)

S228 Figure 32. Actions to manage hyperkalemia (potassium >5.5 mmol/l) in chronic kidney disease

S228 Figure 33. Potassium absorption rates of plant-based, animal-based, and processed foods

S229 Figure 34. Association between estimated glomerular ﬁltration rate (eGFR) and hemoglobin concentration from

general population and high-risk cohorts from the Chronic Kidney Disease Prognosis Consortium, by

diabetes status

S230 Figure 35. Association between estimated glomerular ﬁ ltration rate (eGFR) with serum concentrations of

parathyroid hormone, phosphate, and serum calcium in general population and high-risk cohorts

from the Chronic Kidney Disease Prognosis Consortium, by level of albuminuria (A1–A3)

S233 Figure 36. Risk of all-cause and cardiovascular mortality by estimated glomerular ﬁltration rate (eGFR) and level of

albuminuria from general population cohorts contributing to the Chronic Kidney Disease Prognosis

Consortium

S235 Figure 37. Effect of lowering low-density lipoprotein (LDL) cholesterol per 1.0 mmol/l on risk of major vascular

events by level of estimated glomerular ﬁltration rate (eGFR) at recruitment

S237 Figure 38. Predicted 5-year absolute beneﬁts and harms of allocation to aspirin (A) versus control (C) using a

secondary or primary prevention strategy, by different levels of risk (based on age and sex)

S240 Figure 39. Meta-analyzed adjusted prevalence of atrial ﬁbrillation from cohorts contributing to the Chronic Kidney

Disease Prognosis Consortium, by diabetes status

S241 Figure 40. Strategies for the diagnosis and management of atrial ﬁbrillation

S242 Figure 41. Pooled hazard ratio (HR) comparing non–vitamin K antagonist oral anticoagulants (NOACs) with

warfarin among people with chronic kidney disease in terms of stroke

S243 Figure 42. Pooled hazard ratio (HR) comparing non–vitamin K antagonist oral anticoagulants (NOACs) with

warfarin among people with chronic kidney disease in terms of bleeding

S244 Figure 43. Evidence from (a) randomized controlled trials (RCTs) regarding therapeutic anticoagulation dose by

glomerular ﬁltration rate (GFR) and (b) in areas where RCTs are lacking

S245 Figure 44. Advice on when to discontinue non–vitamin K antagonist oral anticoagulants (NOACs) before

procedures

(low vs. high risk)

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S248 Figure 45. Selected herbal remedies and dietary supplements with evidence of potential nephrotoxicity, grouped

by the continent from where the reports ﬁrst came

S250 Figure 46. Suggested steps in the process of medication review and reconciliation

S251 Figure 47. Essential steps for appropriate sick day rule implementation

S255 Figure 48. Circumstances for referral to specialist kidney care services and goals of the referral

S258 Figure 49. Common symptoms, prevalence, and severity in people with chronic kidney disease

S261 Figure 50. Optimal care model by increasing severity of chronic kidney disease (CKD)

S262 Figure 51. The chronic care model

S262 Figure 52. Speciﬁc components of the chronic kidney disease model of care

S263 Figure 53. Strategy for effective patient education programs for people with chronic kidney disease (CKD)

S264 Figure 54. Telehealth technologies for people with chronic kidney disease (CKD)

S265 Figure 55. The process of transition from pediatric to adult care in chronic kidney disease (CKD)

S269 Figure 56. Relationship between supportive care, comprehensive conservative care, and end-of-life care

S279 Figure 57. Search yield and study ﬂow diagram

SUPPLEMENTARY MATERIAL

Supplementary File (PDF)

Appendix A. Search strategies

Table S1. Search strategies for systematic review topics

Appendix B. Concurrence with Institute of Medicine (IOM) standards for guideline development

Table S2. Guideline development checklist – IOM standards for development of trustworthy clinical practice

guidelines

Appendix C. Data supplement - Summary of ﬁndings (SoF) tables cited in the guideline text

Chapter 1. Evaluation of CKD

Table S3. Adults and children with or without CKD, estimated GFR (eGFR) based on measurements of cystatin C

(eGFRcys); creatinine (eGFRcr); cystatin C and creatinine (eGFRcr-cys) versus measured GFR (mGFR;

using urinary or plasma clearance of exogenous ﬁltration marker)

Table S4. Adults and children with suspected or diagnosed CKD, native kidney biopsy versus clinical or standard

diagnosis or prognosis for studies evaluating diagnostic or prognostic beneﬁt; no comparator for

studies evaluating safety

Table S5. Adults and children, machine-read quantitative or semiquantitative protein or albumin urine dipstick

tests versus laboratory-based methods for measuring urinary protein or albumin (e.g., 24-hour urinary

sample, spot urine protein-to-creatinine ratio [PCR], or albumin-to-creatinine ratio [ACR])

Chapter 2. Risk assessment in people with CKD

Table S6. Adults, children, and young people with CKD G1–G5, C-statistics of kidney failure risk equations for

predicting progression (e.g., Tangri equation [KFRE])

Table S7. Adults, children, and young people with CKD G1–G5, Brier scores of kidney failure risk equations for

predicting progression (e.g., Tangri equation [KFRE])

Table S8. Adults, children, and young people with CKD G1–G5, R

statistics of kidney failure risk equations for

predicting progression (e.g., Tangri equation [KFRE])

Table S9. Adults, children, and young people with CKD G1–G5, sensitivity and speciﬁcity to start kidney

replacement therapy (KRT) for kidney failure risk equations for predicting progression (e.g., Tangri

equation [KFRE])

Chapter 3. Delaying CKD progression and managing its complications

Table S10. Adults and children with CKD, sodium-glucose cotransporter-2 inhibitors (SGLT2i) versus placebo or

usual care; active comparator (e.g., another glucose-lowering agent)

Table S11. Adults and children with CKD and symptomatic hyperuricemia, uric acid–lowering therapy (ULT;

allopurinol, benzbromarone, febuxostat, oxipurinol, pegloticase, probenecid, topiroxostat,

rasburicase, sulﬁnpyrazone, lesinurad) versus active comparator, placebo, or usual care

Table S12. Adults and children with CKD and asymptomatic hyperuricemia, uric acid–lowering therapy (ULT;

allopurinol, benzbromarone, febuxostat, oxipurinol, pegloticase, probenecid, topiroxostat,

rasburicase, sulﬁnpyrazone, lesinurad) versus active comparator, placebo, or usual care

Table S13. Adults and children with CKD and ischemic heart disease, angiography or coronary revascularization

versus medical treatment

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Kidney International (2024) 105 (Suppl 4S), S117–S314

Table S14. Adults and children with CKD and atrial ﬁbrillation, non–vitamin K antagonist oral anticoagulant

(NOAC) with warfarin or NOAC alone versus medical treatment—stroke outcomes

Table S15. Adults and children with CKD and atrial ﬁbrillation, non–vitamin K antagonist oral anticoagulant

(NOAC) with warfarin or NOAC alone versus medical treatment—bleeding outcomes

Appendix D – Data supplement - Summary of ﬁndings (SoF) tables not cited in the guideline text

Chapter 3. Delaying CKD progression and managing its complications

Table S16. Adults and children with CKD but not type 2 diabetes, steroidal mineralocorticoid receptor agonists

(MRAs; canrenone, eplerenone, spironolactone) or non-steroidal MRAs (ﬁnerenone, esaxerenone) versus

active comparator, placebo, or usual care

Table S17. Adults and children with CKD at risk for cardiovascular disease (CVD), aspirin versus placebo

Appendix E – PRISMA diagrams

Chapter 1. Evaluation of CKD

Figure S1. PRISMA diagram for the clinical question “What is the diagnostic and prognostic beneﬁtandsafetyof

kidney biopsy among people with CKD?”

Figure S2. PRISMA diagram for the clinical question “What is the diagnostic accuracy of eGFR based on

measurements of cystatin C, creatinine, or their combination compared to mGFR among people with

and without CKD?”

Figure S3. PRISMA diagram for the clinical question “In children and young adults with suspected or diagnosed

CKD, what is the accuracy of ACR and PCR compared to 24-hour excretion of albumin or protein?”

Figure S4. PRISMA diagram for the clinical question “What is the diagnostic accuracy and reproducibility of POC

blood creatinine compared to laboratory-based tests among people with suspected or diagnosed

CKD?”

Figure S5. PRISMA diagram for the clinical question “What is the diagnostic accuracy of quantitative and

semiquantitative protein or albumin urine dipstick tests compared to laboratory-based tests among

people with suspected or diagnosed CKD?”

Chapter 3. Delaying CKD progression and managing its complications

Figure S6. PRISMA diagram for the clinical question “What is the effect of SGLT2i compared with placebo, usual

care, or an active comparator among people with CKD in terms of mortality, progression of CKD,

complications of CKD, and adverse events?”

Figure S7. PRISMA diagram for the clinical question “What is the effect of MRAs compared with placebo, usual

care, or an active comparator among people with CKD but not type 2 diabetes in terms of mortality,

progression of CKD, complications of CKD, and adverse events?”

Figure S8. PRISMA diagram for the clinical question “What is the effect of glucagon-like peptide-1 (GLP-1)

receptor agonists compared with placebo, usual care, or an active comparator among people with

CKD but not type 2 diabetes in terms of mortality, progression of CKD, complications of CKD, and

adverse events?”

Figure S9. PRISMA diagram for the clinical question “What is the effect of uric acid–lowering therapy compared

with placebo, usual care, or an active comparator among people with CKD and hyperuricemia in terms

of mortality, progression of CKD, complications of CKD, and adverse events?”

Figure S10. PRISMA diagram for the clinical question “What is the effect of aspirin compared to placebo in terms of

the primary prevention of cardiovascular disease (CVD) and safety among people with CKD?”

Figure S11. PRISMA diagram for the clinical question “What are the effects of angiography or coronary

revascularization compared to medical treatment among people with CKD and ischemic heart disease

in terms of mortality, CVD events, kidney failure, and acute kidney injury (AKI)?”

Figure S12. PRISMA diagram for the clinical question

“What

are the effects of NOACs with or without warfarin

compared to placebo or warfarin alone among people with CKD and atrial ﬁbrillation in terms of

stroke and bleeding risks?”

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Kidney International (2024) 105 (Suppl 4S), S117–S314 S123

KDIGO EXECUTIVE COMMITTEE

Garabed Eknoyan, MD

Norbert Lameire, MD, PhD

Founding KDIGO Co-Chairs

Wolfgang C. Winkelmayer, MD, MPH, ScD

Immediate Past Co-Chair

Michel Jadoul, MD

KDIGO Co-Chair

Morgan E. Grams, MD, PhD, MHS

KDIGO Co-Chair

Gloria E. Ashuntantang, MD

Sunita Bavanandan, MBBS

Irene de Lourdes Noronha, MD, PhD

Michelle R. Denburg, MD, MSCE

Joachim H. Ix, MD, MAS

Vivekanand Jha, MD, DM, FRCP, FAMS

Holly Kramer, MD, MPH

Adrian Liew, MD, MBBS, MRCP, FAMS, FASN, FRCP, MClinEpid

Reem A. Mustafa, MD, PhD, MPH

Michelle M. O’Shaughnessy, MB, BCh, BAO, MS, MD

Patrick Rossignol, MD, PhD

Paul E. Stevens, MB, FRCP

Rita S. Suri, MD, MSc

Irma Tchokhonelidze, MD

Marc G. Vervloet, MD, PhD, FERA

Wolfgang C. Winkelmayer, MD, MPH, ScD

Motoko Yanagita, MD, PhD

KDIGO Staff

John Davis, Chief Executive Ofﬁcer

Danielle Green, Executive Director

Melissa Thompson, Chief Operating Ofﬁcer

Michael Cheung, Chief ScientiﬁcOfﬁcer

Amy Earley, Guideline Development Director

Jennifer King, Director of Medical Writing

Tanya Green, Events Director

Coral Cyzewski, Events Coordinator

Kathleen Conn, Director of Communications

KDIGO executive committee www.kidney-international.org

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Reference keys

NOMENCLATURE AND DESCRIPTION FOR RATING GUIDELINE RECOMMENDATIONS

Within each recommendation, the strength of recommendation is indicated as Level 1 or Level 2, and the certainty of the supporting

evidence is shown as A, B, C,orD.

Grade

Implications

Patients Clinicians Policy

Level 1

“We recommend”

Most people in your situation would

want the recommended course of

action, and only a small proportion

would not.

Most patients should receive the

recommended course of action.

The recommendation can be evaluated

as a candidate for developing a policy

or a performance measure.

Level 2

“We suggest”

The majority of people in your situation

would want the recommended course

of action, but many would not.

Different choices will be appropriate for

different patients. Each patient needs

help to arrive at a management

decision consistent with their values

and preferences.

The recommendation is likely to require

substantial debate and involvement of

stakeholders before policy can be

determined.

Grade Certainty of evidence Meaning

A High We are conﬁdent that the true effect is close to the estimate of the effect.

B Moderate The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different.

C Low The true effect may be substantially different from the estimate of the effect.

D Very low The estimate of effect is very uncertain, and often, it will be far from the true effect.

Practice points are consensus-based statements representing the expert judgment of the Work Group and are not graded. They are issued when a

clinical question did not have a systematic review performed, to help readers implement the guidance from graded recommendation (e.g., frequency

of monitoring, provision of standard care [such as regular clinic visits], referral to specialist care, etc.), or for issuing “good practice statements” when

the alternative is considered to be absurd. Users should consider the practice point as expert guidance and use it as they see ﬁt to inform the care of

patients. Although these statements are developed based on a different methodology, they should not be seen as “less important” or a “downgrade”

from graded recommendations.

www.kidney-international.org reference keys

Kidney International (2024) 105 (Suppl 4S), S117–S314 S125

CURRENT CHRONIC KIDNEY DISEASE (CKD) NOMENCLATURE USED BY KDIGO

CKD is deﬁned

as abnormalities of kidney structure or function, present for a minimum of 3 months, with implications for health. CKD is

classiﬁed

based on Cause, Glomerular ﬁltration rate (GFR) category (G1–G5), and Albuminuria category (A1–A3), abbreviated as CGA.

Persistent albuminuria categories

Description and range

GFR categories (ml/min/1.73 m

)

Description and range

≥90

60–89

G3a

45–59

G3b

30–44

15–29

G5 <15Kidney failure

Severely decreased

Moderately to

severely decreased

Mildly to

moderately decreased

Mildly decreased

Normal or high

A2 A3

Normal to mildly

increased

Moderately

increased

Severely

increased

<30 mg/g

<3 mg/mmol

30–300 mg/g

3–30 mg/mmol

>300 mg/g

>30 mg/mmol

KDIGO: Prognosis of CKD by GFR

and albuminuria categories

Green: low risk (if no other markers of kidney disease, no CKD); Yellow: moderately increased risk; Orange: high

risk; Red: very high risk. GFR, glomerular filtration rate.

CKD nomenclature www.kidney-international.org

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CONVERSION FACTORS OF CONVENTIONAL UNITS TO SI UNITS

Conventional unit Conversion factor SI unit

Albumin-to-creatinine ratio (ACR) mg/g 0.113 mg/mmol

Calcium mg/dl 0.2495 mmol/l

Creatinine mg/dl 88.4

mol/l

Protein-to-creatinine ratio (PCR) mg/g 0.113 mg/mmol

Phosphate mg/dl 0.3229 mmol/l

Urate mg/dl 59.48 mmol/l

SI, International System of Units.

Note: Conventional unit  conversion factor ¼ SI unit.

EQUIVALENT ALBUMINURIA CATEGORIES IN CKD

Category AER (mg/24 h)

ACR (approximate equivalent)

Terms(mg/mmol) (mg/g)

A1 <30 <3 <30 Normal to mildly increased

A2 30–300 3–30 30–300 Moderately increased

A3 >300 >30 >300 Severely increased

ACR, albumin-creatinine ratio; AER, albumin excretion rate; CKD, chronic kidney disease.

Relative to the young adult level.

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Kidney International (2024) 105 (Suppl 4S), S117–S314 S127

Abbreviations and acronyms

ACEi angiotensin-converting enzyme inhibitor(s)

ACR albumin-to-creatinine ratio

ADA American Diabetes Association

ADPKD autosomal dominant polycystic kidney disease

AER albumin excretion rate

AIDS acquired immune de ﬁciency syndrome

AKD acute kidney disease

AKI acute kidney injury

ARB angiotensin II receptor blocker

ASCVD atherosclerotic cardiovascular disease

BMI body mass index

BP blood pressure

BSA body surface area

CI conﬁdence interval

CKD chronic kidney disease

CKD-EPI Chronic Kidney Disease Epidemiology

Collaboration

CKiD Chronic Kidney Disease in Children

CKD-MBD chronic kidney disease-mineral and bone

disorder

CKD-PC Chronic Kidney Disease Prognosis

Consortium

CrCl creatinine clearance

CT computed tomography

CVD cardiovascular disease

DALY disability-adjusted life-year

eGFR estimated glomerular ﬁltration rate

eGFRcr creatinine-based estimated glomerular

ﬁltration rate

eGFRcr-cys creatinine and cystatin C–based estimated

glomerular ﬁltration rate

eGFRcys cystatin C–based estimated glomerular

ﬁltration rate

EKFC European Kidney Function Consortium

EMA European Medicines Agency

EMR electronic medical record

ERT Evidence Review Team

FDA Food and Drug Administration

GBD Global Burden of Disease

GFR glomerular ﬁltration rate

GLP-1 RA glucagon-like peptide-1 receptor agonist(s)

GN glomerulonephritis

HBV hepatitis B virus

HCV hepatitis C virus

HDL high-density lipoprotein

HIV human immunodeﬁciency virus

HR hazard ratio

HRQoL health-related quality of life

IgG immunoglobulin G

IQR interquartile range

i.v. intravenous

KDIGO Kidney Disease: Improving Global

Outcomes

KDOQI Kidney Disease Outcomes Quality Initiative

KFRE Kidney Failure Risk Equation

KRT kidney replacement therapy

LDL low-density lipoprotein

LMIC low- and middle-income countries

MACE major adverse cardiovascular events

MDRD Modiﬁcation of Diet in Renal Disease

mGFR measured glomerular ﬁltration rate

MRA mineralocorticoid receptor antagonist(s)

mTOR mammalian target of rapamycin

NICE National Institute for Health and Care

Excellence

NIHR National Institute for Health and Care

Research

NOAC non–vitamin K antagonist oral

anticoagulant

NSAIDs nonsteroidal anti-inﬂammatory drugs

OR odds ratio

OTC over-the-counter

PCR protein-to-creatinine ratio

PCSK-9 proprotein convertase subtilisin/kexin type-9

PICOS population, intervention, comparator,

outcomes, study design

POCT point-of-care testing

PROM patient-reported outcome measure

QoL quality of life

RAS(i) renin-angiotensin system (inhibitor)

RAAS(i) renin-angiotensin-aldosterone system

(inhibitor)

RBC red blood cell

RCT randomized controlled trial

RR relative risk

SCr serum creatinine

SBP systolic blood pressure

SES socioeconomic status

SGLT2i sodium-glucose cotransporter-2

inhibitor(s)

T1D Type 1 diabetes

T2D Type 2 diabetes

UK United Kingdom

US United States

USRDS United States Renal Data System

WHO World Health Organization

abbreviations and acronyms www.kidney-international.org

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Kidney International (2024) 105 (Suppl 4S), S117–S314

Notice

SECTION I: USE OF THE CLINICAL PRACTICE GUIDELINE

This Clinical Practice Guideline document is based upon literature searches conducted from July 2022 throug h April 2023 and

updated in July 2023. It is designed to assist decision-making. It is not intended to deﬁne a standard of care and should not be

interpreted as prescribing an exclusive course of management. Variations in practice will inevitably and appropriat ely occur

when clinicians consider the needs of individual patients, available resources, and limitations unique to an institution or type of

practice. Healthcare providers using the statements in this document (both practice points and recommendations) should

decide how to apply them to their own clinical practice.

SECTION II: DISCLOSURE

Kidney Disease: Improving Global Outcomes (KDIGO) makes every effort to avoid any actual or reasonably perceived conﬂicts

of interest that may arise from an outside relationship or a personal, professional, or business interest of a member of the Work

Group. All members of the Work Group are required to complete, sign, and submit a disclosure and attestation form showing

all such relationships that might be perceived as or are actual conﬂicts of interest. This document is updated annually, and

information is adjusted accordingly. All reported information is published in its entirety at the end of this document in the

Work Group members’ Disclosure section and is kept on ﬁle at KDIGO.

International Society of Nephrology. This is an open access article under the CC BY-NC-ND license (http://

creativecommons.org/licenses/by-nc-nd/4.0/). Single copies may be made for personal use as allowed by national

educational use. No part of this publication may be reproduced, amended, or transmitted in any form or by any means,

electronic or mechanical, including photocopying, recording, or any information storage and retr ieval system, without

explicit permission in writing from KDIGO. Details on how to seek reprints, permission for reproduction or translation, and

further information about KDIGO’s permissions policies can be obtained by contacting Melissa Thompson, Chief Operating

Ofﬁcer, at melissa.th ompson@kdigo.org.

Neither KDIGO, Kidney International, the Publisher, nor the authors, contributors, or editors shall have or assume any

liability for any direct, indirect, incidental, special, exemplary, or consequential damages (including without limitation lost

proﬁts) or any injury and/or damage to persons or property, however caused and on any theory of liability, whether in

contract, strict liability, or tort (includi ng product liability, negligence or otherwise) arising in any way out of the use or

operation of any methods, products, instructions, or ideas contained in the material herein.

www.kidney-international.org notice

Kidney International (2024) 105 (Suppl 4S), S117–S314 S129

Foreword

Kidney International (2024) 105 (Suppl 4S), S117–S314; https://doi.org/10.1016/j.kint.2023.10.018

Copyright ª 2023, Kidney Disease: Improving Global Outcomes (KDIGO). Published by Elsevier Inc. on behalf of the International Society of Nephrology. This is an open access

article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

The Kidney Disease: Improving Global Outcomes (KDIGO)

organization was established in 2003 with the mission to

improve the care and outcomes of people living with kidney

disease worldwide. The development and implementation of

global clinical practice guidelines is central to the many ac-

tivities of KDIGO to fulﬁll its mission. Twenty years later, we

are excited to present this update of the KDIGO Clinical

Practice Guideline for the Evaluation and Management of

Chronic Kidney Disease (CKD) to complement the existing

12 guidelines that address various other facets of kidney

disease management.

Our aspiration is that the KDIGO CKD Guideline serves as

a comprehensive reference for evidence-based practices, of-

fering clear and valuable guidance for the optimal diagnosis

and treatment of CKD. The updated guideline is the result of

a rigorous process, extensively detailed in the KDIGO

Methods Manual. To promote objectivity and transparency,

we screen Guideline Co-Chairs and Work Group members

(which include clinicians, researchers, and patients) for con-

ﬂicts of interest. Over a span of 2–3 years, these individuals

volunteer their time, starting with the creation of a Scope of

Work that undergoes an open public review to engage all

stakeholders. This docu ment is then adapted into a Request

for Proposal, which is used to enlist an independent Evidence

Review Team.

The Evidence Review Team conducts a systematic review of

existing literature, extracting studies with appropriate design

and outcomes deemed important by both people with CKD

and clinicians. All work is meticulously graded on study

quality and potential bias, forming the basis for quantifying

the overall certainty of the evidence using the “Grading of

Recommendations Assessment, Development, and Evalua-

tion” (GRADE) approach. The penultimate version of the

guideline also undergoes public review to capture additional

perspectives. Thus, guidelines are the result of a rigorous and

objective assessment of available evidence, enriched by the

collective expertise of healthcare providers, researchers, and

patients al ike. Guideline statements (“We recommend” or

“We suggest”)reﬂect clinical questions that were addressed by

the evidence reviews from the Evidence Review Team. Practice

points provide guidance on clinical questions that were not,

and largely could not be, studied by the Evidence Review

Team.

We view the current guideline as a dynamic, evolving

resource rather than a static document. We are delighted by the

recent pace of clinical discovery that substantially increased the

scientiﬁc basis of optimal CKD diagnosis and management,

and we remain committed to updating recommendations and

practice points as important evidence emerges. We hope that

the guideline will serve as a useful tool for clinicians in their

daily practice, prov iding clear insight into the evidence-based

recommendations while highlig hting areas requiring further

research. Ultimately, our aim is to facilitate more effective and

consistent care to patients with CKD worldwide, and the

publication of the CKD Guideline will provide the foundation

of many dissemination and implementation activities to in-

crease the outreach and usefulness of this work.

We extend our heartfelt g ratitude for all those who have

contributed to the CKD Guideline. First, to the members of

the Methods Committee, particularly Dr. Marcello Tonelli,

MD, SM, MSc, Chair of the Committee, and Amy Earley, BS,

KDIGO Guideline Development Director, for setting the

expectation of rigor, balance, and transparency throughout

the process. Next, to the Evidence Review Team at Johns

Hopkins University, for their meticulous work in reviewing

the existing literature. Third, to the Work Group members,

led by the indefatigable Drs. Adeera Levin, MD, and Paul

Stevens, MB, for their diligence and innumerable hours vol-

unteered to shepherd the guideline to publication. Fourth, to

the many individuals who provided comments during the

rounds of public revie w. Finally, to the whole KDIGO staff,

for their steadfast, behind the scenes commitment to excel-

lence in patient care.

Sincerely,

Morgan E. Grams, MD, PhD, MHS

Michel Jadoul, MD

KDIGO Co-Chairs

foreword www.kidney-international.org

S130

Kidney International (2024) 105 (Suppl 4S), S117–S314

Work Group membership

WORK GROUP CO-CHAIRS

Paul E. Stevens, MB, FRCP, RCPathME

East Kent Hospitals University

NHS Foundation Trust

Canterbury, United Kingdom

Adeera Levin, MD, FRCPC

University of British Columbia

Vancouver, Canada

WORK GROUP

Soﬁa B. Ahmed, MD, MMSc, FRCPC

University of Alberta

Edmonton, Alberta, Canada

Juan Jesus Carrero, Pharm, PhD Pharm, PhD Med,

MBA, FNKF, FERA

Karolinska Institutet

Stockholm, Sweden

Bethany Foster, MD, MSCE

McGill University

Montreal, Quebec, Canada

Anna Francis, MBBS, FRACP, CF, MMed, PhD

Queensland Children’s Hospital

Brisbane, Australia

Rasheeda K. Hall, MD, MBA, MHS

Duke School of Medicine

Durham, North Carolina, USA

Will G. Herrington, MA, MBBS, MD, FRCP

University of Oxford

Oxford, United Kingdom

Guy Hill

Manchester, United Kingdom

Lesley A. Inker, MD, MS, FRCP(C)

Tufts Medical Center

Boston, Massachusetts, USA

Rümeyza Kazancıo



glu, MD

Bezmialem Vakif University

Istanbul, Turkey

Edmund Lamb, PhD, FRCPath

East Kent Hospitals University NHS

Foundation Trust

Canterbury, United Kingdom

Peter Lin, MD, CCFP

Canadian Heart Research Center

Toronto, Ontar io, Canada

Magdalena Madero, MD

Instituto Nacional de Cardiología Ignacio Chavéz

Mexico City, Mexico

Natasha McIntyre, PhD

Western University

London Health Sciences Centre-Victoria Hospital

London, Ontario, Canada

Kelly Morrow, MS, RDN, CD, FAND

Basty r University, Osher Center for Integrative

Medicine University of Washington

Kenmore, Washington, USA

Glenda Roberts

UW Center for Dialysis Innovation &

Kidney Research Institute

Seattle, Washington, USA

Dharshana Sabanayagam, MD, FRACP

University of Sydney

Sydney, Australia

Elke Schaeffner, MD, MSc

Charité Universitätsmedizin Berlin

Berlin, Germany

Michael Shlipak, MD, MPH

University of California, San Francisco

San Francisco, California, USA

Rukshana Shroff, MD, FRCPCH, PhD

UCL Great Ormond Street Hospital Institute of Child Health,

London, United Kingdom

Navdeep Tangri, MD, PhD, FRCP(C)

University of Manitoba

Winnipeg, Manitoba, Canada

Teerawat Thanachayanont, MD, MSc

Bhumirajanagarindra Kidney Institute

Bangkok, Thailand

Ifeoma Ulasi, MBBS, FWACP, PGD, MSc

University of Nigeria, Ituku-Ozalla Campus

Enugu, Nigeria

www.kidney-international.org Work Group membership

Kidney International (2024) 105 (Suppl 4S), S117–S314 S131

Germaine Wong, MD, PhD

University of Sydney

Sydney, Australia

Chih-Wei Yang, MD

Chang Gung University

Taoyuan, Taiwan

Luxia Zhang, MD, MPH

Peking University First Hospital

Beijing, China

METHODS COMMITTEE REPRESENTATIVE

Bertram L. Kasiske, MD, FACP

Hennepin County Medical Center

University of Minnesota

Minneapolis, MN, USA

EVIDENCE REVIEW TEAM

The Johns Hopkins University Evidence-based Practice Center

Karen A. Robinson, PhD, Professor of Medicine

Lisa Wilson, ScM, Research Associate

Renee F. Wilson, MS, Research Associa te

Dipal M. Patel, MD, PhD, Assistant Professor of Medicine

Troy Gharibani, BS, BA, Research Assistant

Xuhao Yang, MSPH, Research Assistant

Verna Laz ar, MBBS, MPH, Research Assistant

Jeongmin Hana Kim, PharmD, MSc, Research Assistant

Work Group membership www.kidney-international.org

S132

Kidney International (2024) 105 (Suppl 4S), S117–S314

Abstract

The Kidney Disease: Improving Global Outcomes (KDIGO) 2024 Clinical Practice Guideline for

the Evaluation and Management of Chronic Kidney Disease (CKD) is an update to the KDIGO

2012 guideline on the topic. The aim is to assist clinicians caring for people with CKD, both

adults and children. People receiving dialysis and kidney transplant recipients are not the focus of

this guideline. The scope includes chapters dedicated to the evaluation of CKD, risk assessment in

people with CKD, manage ment to delay CKD progression and manage its complications, medical

management and drug stewardship in CKD, and optimal models of CKD care. In addition, this

guideline includes a comprehensive introduction from the guideline Co-Chairs, a patient

foreword, a discussion of special population considerations, a presentation of the relative and

absolute risks associated with speciﬁc outcomes from the CKD Prognosis Consortium (CKD-

PC), and an extensive section dedicated to research recommendations based on the current gaps

in evidence. The goal of the guideline is to generate a useful resource for clinicians and patients by

providing actionable recommendations based on a rigorous formal evidence review, practice

points that serve to direct clinical care or activities for which a systematic review was not con-

ducted, and useful infographics. The guideline targets a broad audience of healthcare providers

involved in the care of people with CKD as well as people with CKD themselves while being

mindful of implications for policy and payment. Development of this guideline update followed

an explicit process of evidence review and appraisal. Treatment approaches and guideline rec-

ommendations are based on systematic reviews of relevant studies, and appraisal of the certainty

of the evidence and the strength of recommendations followed the “Grading of Recommenda-

tions Assessment, Development, and Evaluation” (GRADE) approach. Limitations of the evi-

dence are discussed, with areas of future research also presented.

Keywords: chronic kidney disease; CKD; evaluation; guideline; KDIGO; management

CITATION

In citing this document, the following format should be used: Kidney Diseas e: Improving

Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for

the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):

S117–S314.

www.kidney-international.org abstract

Kidney International (2024) 105 (Suppl 4S), S117–S314 S133

Patient foreword

The identiﬁcation of chronic kidney disease (CKD) begins a

long journey for any patient that will have a direct impact on

their lifestyle and future health outcomes. This guideline

identiﬁes the suitability of medical interventions that can

improve or delay the ser iousness of CKD and possible kidney

failure.

In a complicated world of health provision, having a set of

evidential recommendations and practice points provides

kidney service providers with the targets for a quality CKD

service for people with kidney disease. However, if the starting

point for many people is ignorance of what a kidney actually

does, then without a holistic approach to patient care, much of

the potential effectiveness of medical interventions can be

diluted because of patient circumstances and psychological

challenges.

Acceptance of the seriousness of CKD can take a lot

longer for a person to process, to the possible detr iment of

medical intervention, and may well lead to issues over

adherence.

A controlled, managed CKD decline is so beneﬁcial to

patients who have so many social issues to contend with, be it

diet, tiredness, liquid control, pill overload, and a deep dive

into the very mechanics of how we eat and drink to survive

and excrete excesses.

In an ever-increasingly busy world of medical care, as pa-

tients, we believe that the best approach is for any physician to

aim to achieve a partnership of knowledge with the patient

regarding their CKD care. This will build patient conﬁdence and

self-awareness, with the aim that any patient who sadly arrives at

possible dialysis is in the right state of mind, which is critical for a

considered approach to the next stage of a patient’s journey.

Guy Hill

CKD Work Group Member

patient foreword www.kidney-international.org

S134

Kidney International (2024) 105 (Suppl 4S), S117–S314

Introduction, qualifying statements, and key concepts

This 2024 update of the KDIGO Clinical Practice Guideline

for the Evaluation and Management of Chronic Kidney Dis-

ease (CKD)

is an evidence-based guideline that provides

recommendations and practice points for clinical

management activities.

The past 10 years have provided new hope for improved

treatment of CKD. A greater under standing of healthy lifestyle

and lifestyle modiﬁcations together with new medications

and technologies furnish improved options for treatment and

monitoring of CKD. People with CKD, healthcare providers,

and health systems are eager to implement these advances in

the most effective and evidence-based manner. This requires

integration of new therapies with lifestyle management and

existing medications using approaches that engage patients

and optimize application of health resources. The goal of this

guideline document is to provide such guidance. The majority

of statements from the 2012 guideline have been updated

based on current knowledge and practice. Only 6 statements

were retained in their original form in 2012.

As Co-Chairs, we would like to recognize the outstanding

efforts of the Work Group, the Evidence Review Team (ERT),

and Kidney Disease: Improving Global Outcomes (KDIGO)

staff. The Work Group was diverse, multinational, multidis-

ciplinary, experienced, thoughtful, and dedicated. Notably,

the Work Group included 2 members who have CKD who

contributed actively as peers to keep the guideline relevant

and patient-centered. We are indebted to each and every in-

dividual who contributed to this process. We hope that the

guidance provided here will help improve the care of people

with CKD worldwide.

The KDIGO 2012 CKD guideline was built on the United

States (US)-based Kidney Disease Outcomes Quality Initiative

(KDOQI) 2002 Guideline on Deﬁnition, Classiﬁcation, and

Evaluation of CKD,

accepted by the international

community in 2005. It reinforced the deﬁnition of CKD

incorporating a persistent reduction in glomerular ﬁltration

rate (GFR) and markers of kidney damage and modiﬁed the

staging and classiﬁcation system to include elements that

had begun to be appreciated by the clinical community.

Speciﬁcally, the 2012 guideline introduced the concept of a

“CGA” classiﬁcation of CKD based on cau se (C), level of

kidney function determined by GFR (G), and degree of

albuminuria (A). The CGA classiﬁcation laid a foundation

upon which management, treatment, research, and risk

assessment of CKD have since been based.

The deﬁnition, staging, and classiﬁcation of CKD pro-

posed by the KDIGO 2012 CKD guideline have been widely

accepted and implemented worldwide. Research has since

highlighted that higher speciﬁc stages or categories of CKD,

characterized by level of GFR and albuminuria independently,

portend greater relative risk (RR) for adverse outcomes.

4–7

These include, but are not limited to, CKD progression,

cardiovascular disease (CVD), mortality (all-cause and car-

diovascular), kidney failure, and acute kidney injury (AKI).

The development of risk-prediction tools has reﬁned moni-

toring and referral to specialist nephrology and has aided in

the estimation of prognosis.

6,8–10

Although there remains

ongoing discussion about appli cation of the same thresholds

to deﬁne disease in older adults,

it is still clear that even

in older populations, risk of adverse outcomes increases

with higher CKD stages (Figure 1).

In any ﬁeld of

medicine, although data from large population studies

inform clinical practice guidelines and associated

recommendations for care, it is critically important to

consider the individual in front of you, their preferences,

and their individual risks and beneﬁts. We recognize that

the threshold GFR <60 ml/min per 1.73 m

(GFR

categories G3a–G5) for >3 months to indicate a diagnosis

of CKD is well below the average in young adult men and

women,

but because a signiﬁcant GFR reduction in

younger people is also usually associated w ith other markers

of kidney disease, the diagnosis of CKD would be captured.

Similarly, we recognize that there is an average age-

associated GFR decline observed in longitudinal and cross-

sectional studies,

but with substantial variation amon g

individuals within the population,

such that not all

individuals will have a signiﬁcant GFR decline with age.

This guideline is not intended to be a textbook, and thus

statements regarding prevention and screening for CKD,

although important topics, are not addressed in depth but are

brieﬂy discussed below in the context of the global burden of

CKD and in Chapter 1. For a more detailed discussion of these

issues, we refer readers to existing textbooks and reviews.

16–18

Prevention and screening for CKD should be conducted

mostly by healthcare providers in primary care and in other

specialties, such as endocrinology, cardiology, and oncology,

rather than restricted to nephrologists. We strongly support

efforts aimed at the early detection and treatment of CKD

among people at high risk for CKD, including those with

hypertension, diabetes, and CVD. Screening efforts in these

and other populations should include assessments of GFR

(estimated or in certain situations measured [see Section 1.2]

and albuminuria [or surrogate, see Section 1.3]).

The intended starting point for this update of the KDIGO

2012 CKD guideline is an established diagnosis of CKD,

though there are some practice points to clarify the evaluation

of CKD and the ascertainment of chronicity. The care of

people with CKD is multifaceted and complex. Several critical

aspects of this comprehensive care, such as blood pressure

(BP), diabetes, and lipid management, have been addressed in

other KDIGO guidelines. These topics were not reviewed for

the current guideline, but recommendations have been

incorporated where relevant and we refer readers to those

speciﬁc KDIGO guidelines and their updates.

19–23

www.kidney-international.org introduction, qualifying statements, and key concepts

Kidney International (2024) 105 (Suppl 4S), S117–S314 S135

This clinical practice guideline includes 2 different types of

statements: graded recommendations, which are supported by

systematic reviews (i.e., de novo reviews conducted by the in-

dependent ERT or existing high-quality reviews that have been

systematically identiﬁed), and ungraded practice points, which

serve to direct clinical care or activities for which a systematic

review was not conducted for various reasons (e.g., lack of a

sufﬁcient evidence base or randomized controlled trials

[RCTs] would be impractical/unethical). Both recommenda-

tions and practice points are intended to help guide clinical

practice and aid in decision-making; thus, they collectively are

the guidance statements. They are clearly articulated and

presented together so that all guideline statements can be

implemented. The distinction between them is based on the

process by which they are derived, that process is based on the

framework methodology from the KDIGO Methods Com-

mittee and aligns with other international guideline groups

utilizing the “Grading of Recommendations Assessment,

Development, and Evaluation” (GRADE) methodology.

Several exciting developments have been introduced into

clinical practice since the KDIGO 2012 CKD guideline was

published. These include reﬁnement of evaluation of GFR,

population and individual risk prediction, and novel treat-

ments which have all positively inﬂuenced the prognosis for

people with CKD. The Work Group has aimed to generate a

guideline that is both rigorously devoted to new and existing

evidence, and clinically useful.

Research recommendations are presented in a separate

section at the end of this document and are intended to guide

the next set of important research questions to inform and

improve outcomes of people living with CKD. The research

recommendations are not exhaustive but are intended to help

focus the clinical and research communities on unanswered

questions including improving diagnostic tools and evalua-

tion of kidney function, development and testing of risk

prediction equations in clinical and research settings, evalu-

ation of different therapies to delay progression in various

combinations, improved medication management, and

optimal models of care. We speciﬁcally urge the community

to be in clusive of people across the lifecycle and include sex

and ge nder, and etiology of CKD, as important variables in all

studies.

Age <65

eGFRcr-cys <10 10–29 30–299 300+ <10 10–29 30–299 300+

105+ 0.99 1.2 1.5 2.4 0.93 1.0 1.1 2.6

90–104 ref 1.3 1.5 2.5 ref 1.2 1.3 1.9

60–89 1.2 1.6 2.0 2.9 1.3 1.4 1.6 2.1

45–59 2.1 2.7 2.9 4.5 1.8 2.6 3.1 3.5

30–44 2.7 3.8 4.2 5.6 1.9 2.3 3.0 3.9

<30 5.2 4.0 7.1 8.6 4.1 3.6 4.7 5.8

105+ 0.95 1.4 1.7 4 0.96 1.2 1.6 2.7

90–104 ref 1.6 1.8 3.5 ref 1.2 1.5 2.2

60–89 1.3 1.7 2.3 3.9 1.2 1.4 1.7 2.6

45–59 2.5 4.0 4.6 6.0 1.9 2.0 2.5 3.8

30–44 3.1 6.6 5.3 7.1 2.6 3.7 3.5 3.5

<30 6.0 5.5 9.4 12 2.6 2.9 5.1 5.1

105+ 0.57 0.77 2.3 12 0.86 1.1 1.7 3.4

90–104 ref 1.4 3.9 11 ref 1.3 1.5 3.0

60–89 1.9 3.7 8.3 33 1.2 1.7 2.1 3.6

45–59 7.0 16 28 100 1.7 3.3 3.4 5.3

30–44 22 34 109 210 3.5 4.3 6.8 5.7

<30 335 267 419 625 7.5 6.3 9.7 8.9

105+ 0.75 1.0 1.4 3.4 0.93 1.0 1.3 1.9

90–104 ref 1.2 1.8 2.6 ref 1.2 1.4 2.3

60–89 1.6 2.7 2.9 5.8 1.1 1.3 1.5 1.8

45–59 4.2 6.0 5.6 7.6 1.5 2.0 2.1 2.6

30–44 5.7 9.4 9.8 9.4 1.8 2.4 3.0 2.8

<30 15 14 14 13 3.7 2.9 4.3 5.4

105+ 1.0 1.1 1.1 1.5 0.93 1.9 1.5 2.6

90–104 ref 1.1 1.2 1.3 ref 1.8 2.1 3.9

60–89 1.1 1.2 1.3 1.6 1.2 2.1 2.2 5.4

45–59 1.3 1.7 1.5 2.0 3.2 7.3 3.4 8.4

30–44 1.5 1.8 1.6 2.1 6.5 9.1 6.6 13

<30 2.1

2.4 2.4 3.5 1.4 7.6 18 16

esaesid yretra larehpirePnoitazilatipsoH

Kidney failure replacement therapy Heart failure

ekortSytilatrom ralucsavoidraC

noitcrafni laidracoyMytilatrom esuac-llA

+56 egAg/gm ,RCAg/gm ,RCA

eGFRcr-cys <10 10–29 30–299 300+ <10 10–29 30–299

105+ 1.2 1.4 1.9 3.5 0.97 1.4 2.0

90–104 ref 1.2 1.4 2.0 ref

1.2 1.1

60–89 1.2 1.5 1.8 2.3 1.1 1.4 1.5

45–59 1.6 2.0 2.4 2.9 1.6 1.9 2.3

30–44 2.0 2.4 3.2 4.1 2.1 2.6 3.1

<30 3.4 4.1 5.1 6.5 4.9 3.0 5.1

105+ 1.1 1.5 2.0 12 1.2 1.3 1.5

90–104 ref 1.4 1.4 3.4 ref 1.3 1.3

60–89 1.2 1.7 2.2 3.1 1.1 1.4 1.8

45–59 1.7 2.4 3.0 4.3 1.5 1.7 2.0

30–44 2.4 3.1 4.5 5.8 1.5 2.0 2.1

<30 5.7 5.2 5.1 7.8 1.7 2.0 2.4

105+ 2.0 1.0 2.1 0.99 1.5 1.7

90–104 ref 1.9 4.7 10 ref 1.3 1.5

60–89 1.4 2.6 6.2 19 1.2 1.5 2.0

45–59 3.7 7.9 16 42 1.6 2.0 2.9

30–44 14 14 46 137 2.3 2.9 3.5

<30 87 364 241 406 4.4 4.1 5.5

105+ 0.91 1.1 1.3 1.9 0.95 1.1 1.0

90–104 ref 1.3 1.4 3.9 ref 1.2 1.3

60–89 1.5 2.1 2.7 4.7 1.1 1.2 1.5

45–59 3.6 4.3 5.1 7.3 1.2 1.4 1.7

30–44 5.7 5.9 7.2 9.8 1.5 1.8 2.0

<30 10 11 11 22 1.8 1.8 2.2

105+ 1.0 1.1 1.2 2.2 1.1 2.3 2.9

90–104 ref 1.1 1.3 1.4 ref 1.3 2.0

60–89 1.1 1.2 1.3 1.5 1.3 1.6 2.0

45–59 1.2 1.2 1.4 1.6 2.0 2.8 3.1

30–44 1.5 1.4 1.6 2.0 3.5 2.8 3.8

<30 1.9 1.9 2.0 2.6 8.4 4.1 5.9

esaesid yretra larehpirePnoitazilatipsoH

Kidney failure replacement therapy Heart failure

ekortSytilatrom ralucsavoidraC

noitcrafni laidracoyMytilatrom esuac-llA

g/gm ,RCAg/gm ,RCA

300+

1.9

3.4

3.8

5.0

3.3

2.8

2.5

2.3

4.8

7.0

2.2

3.2

4.1

6.1

7.2

3.7

2.4

2.0

1.9

2.2

3.2

4.9

4.8

3.2

3.1

5.9

Figure 1 | Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by creatinine and cystatin C

(eGFRcr-cys) and albumin-to-creatinine ratio (ACR) categories and risks for 10 common complications by age in multivariable-adjusted

analyses. Numbers reﬂect the adjusted hazard ratio compared with the reference cell. Adjustment variables included age, sex, smoking status

(current, former, or never), systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, body mass index, use of

antihypertensive medications, and a medical history of diabetes, coronary heart disease, stroke, heart failure, atrial ﬁbrillation, peripheral artery

disease, cancer, and chronic obstructive pulmonary disease, where relevant. The colors were determined for each outcome separately using the

following rule: the percentile shaded the darkest green color corresponds to the proportion of cells in the grid without CKD (e.g., 6 of 24 cells),

and the percentile shaded the darkest red color corresponds to proportion expected to be at highest risk (e.g., 5 of 24 cells). In this manner, the

numbers of green and red cells are consistent across outcomes, but the patterns are allowed to differ. ref, reference cell. Reproduced with

permission from JAMA, Writing Group for the CKD Prognosis Consortium; Grams ME, Coresh J, Matsushita K, et al. Estimated glomerular ﬁltration

rate, albuminuria, and adverse outcomes: an individual-participant data meta-analysis. JAMA. 2023;330(13):1266–1277.

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Kidney International (2024) 105 (Suppl 4S), S117–S314

Deﬁnition and classiﬁcation of CKD

Deﬁning CKD.

CKD is deﬁned as abnormalities of kidney

structure or function, present for a minimum of 3 months,

with implications for health (Table 1).

Classifying CKD. CKD is classiﬁed based on Cause, GFR

category (G1–G5), and Albuminuria category (A1–A3),

abbreviated as CGA.

These 3 components of the

classiﬁcation system are each critical in the asse ssment of

people wit h CKD and help enable determination of severity

and risk. Listed below are reference tables describing each

component. Note that while the deﬁnition of CKD includes

many different markers of kidney damage and is not

conﬁned to decreased GFR and albumin-to-creatinine ratio

(ACR) >30 mg/g [>3 mg/mmol], the classiﬁcation system

is based on the 2 dimensions of GFR and degree of

albuminuria (Tables 2 and 3). This nuance is often missed

by healthcare providers and students.

It is well established that patient advocates with CKD and

healthcare providers prefer the more clinically useful and

generally understood assessment of GFR resulting from the

use of GFR estimating equations compared with serum

creatinine (SCr) alone. Globally, although still not universally

available in all countries, SCr is measured routinely and the

approach to assessment of GFR is therefore to use SCr and an

estimating equation for initial assessment of GFR. The

approach to evaluation of GFR using initial and supportive

tests is described in greater detail in Chapter 1.

Etiology of CKD should be sought, and there are

numerous systems fo r grouping various etiologies, some of

which are evolving with new knowledge and diagnostic tools.

There are congenital and genetic causes of CKD, some asso-

ciated with systemic diseases, and others that are primary. It is

beyond our remit to suggest a speciﬁc approach, but we

highlight the importance of establishing a cause to individ-

ualize management of CKD.

The global burden of CKD

The Global Burden of Disease, Injuries, and Risk Factors

Study (GBD) pulls together data on premature death and

disability from more than 350 diseases and injuries in 204

countries, by age and sex, from 1990 to the present.

Disease

“burden” is the impact of a health problem as measured by

ﬁnancial cost, mortalit y, morbidity, or other indicators and

can be measured by combining 2 indicators to descr ibe the

disability-adjusted life-years (DALYs): the number of years

of life lost to disease and the number of years lived with

disability due to disease.

Globally, in 2017, a systematic analysis from the all-age

GBD project found 697.5 million (95% uncertainty interval

[UI]: 649.2–752.0) cases of all-stage CKD, for a global preva-

lence of 9.1% (8.5%–9.8%).

By 2021, a joint statement from

the American Society of Nephrology, European Renal

Association, and International Society of Nephrology

indicated that more than 850 million people suffer from

some form of kidney disease, roughly double the number of

people who live with diabetes (422 million) and 20 times

more than the prevalence of cancer worldwide (42 million)

or people living with AIDS/HIV (36.7 million). These

estimates derive from aggregation of studies worldwide,

which have applied a variety of deﬁnitions of CKD;

nevertheless, they furnish the best guide about global CKD

prevalence.

In 2017, CKD was estimated to account for 35.8 million

(95% UI: 33.7e38.0) DALYs, and 1.2 million people died

from CKD. Most of the burden of CKD was concentrated in

the 3 lowest quintiles of sociodemographic index (SDI). In

2019, CKD was responsible for 41.5 million (95% UI: 38.3–

45.0) DALYs, and 1.43 million people died from CKD.

Age-

standardized DALY rates (Figure 2

) were highest in central

and Andean Latin America, at 1348.1 (1203.6–1521.6) and

836.3 (704.2–981 .6) per 100,000, respectively (global rate

was 514.9 [474.9–558.9]). In 2017, CKD in diabetes

represented a third of all DALYs, and there were 1.4 million

Table 1 | Criteria for chronic kidney disease (either of the

following present for a minimum of 3 months)

Markers of kidney

damage (1 or more)

Albuminuria (ACR $30 mg/g [$3 mg/mmol])

Urine sediment abnormalities

Persistent hematuria

Electrolyte and other abnormalities due to

tubular disorders

Abnormalities detected by histology

Structural abnormalities detected by imaging

History of kidney transplantation

Decreased GFR GFR <60 ml/min per 1.73 m

(GFR categories G3a–G5)

ACR, albumin-to-creatinine ratio; GFR, glomerular ﬁltration rate.

Table 2 | GFR categories in CKD

GFR

Category

AER

(mg/24 h)

ACR (approximately

equivalent)

Terms(mg/mmol) (mg/g)

A1 <30 <3 <30 Normal to mildly

increased

A2 30–300 3–30 30–300 Moderately increased

A3 >300 >30 >300 Severely increased

ACR, albumin-to-creatinine ratio; AER, albumin excretion rate.

Relative to the young adult level.

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Kidney International (2024) 105 (Suppl 4S), S117–S314 S137

(95% UI: 1.2–1.6) CVD-related deaths in peop le with CKD;

25.3 (22.2–28.9) million CVD DALYs were attributable to

impaired kidney function. Overall, CKD and its effect on

CVD resulted in 2.6 million (95% UI: 2.4–2.8) deaths in

2017 and CKD has risen from 19th to 11th in rank among

leading causes of death between 1990 and 2019 due to

aging and an increasing burden of risk factors for CKD

(including diabetes and hypertension) that, together,

contribute to more than half of the deaths from CKD.

Screening and prevention

Despite the increasing recognition of the true burden of CKD,

there remains controversy and lack of consensus as to the

utility of population screening for CKD

or targeted

screening programs,

due to the complexity of the

underlying sociopolitical and resource environment. Public

health policy has a role to play in identifying and

addressing risk factors to prevent CKD, to identify CKD

early, and to delay its progression and associated adverse

outcomes. Education of both health personnel and the

populations at risk, implementation of early kidney disease

detection programs, and incorporation of evidence-based

treatment of CKD and its associated conditions, such as BP

and diabetes, are all essential components of a strategy to

address this burden. A systematic review suggested that

screening for CKD is cost-effective in people with diabetes

and hypertension, the 2 most common causes of CKD

worldwide.

However, clinical trials have not been

conducted to determine whether or not an intervention to

detect, risk-stratify, and treat CKD would improve the

health outcomes for the targeted population. Nevertheless,

cost-effective analysis of population-wide screening for CKD

incorporating evidence-based treatment with sodium-

glucose cotransporter-2 inhibitors (SGLT2i) recently

concluded that screening adults for albuminuria to identify

CKD could be cost-effective in the United States.

This evidence aligns with the KDIGO Controversies Con-

ference on Early Detection and Intervention in CKD, which

concluded that early identiﬁcation of CKD in people at risk,

who are usually asymptomatic, would likely be beneﬁcial in the

community and primary care settings if the programs are

interwoven with risk stratiﬁcation and treatment.

community program must be able to provide treatment to

the high-risk group of patients with newly detected CKD to

justify systematic early detection strategies. An additional

conclusion was that screening and treatment programs for

CKD should be implemented based on risk stratiﬁcation to

prioritize people, particularly in settings with limited

economic resources. Although globally people with

hypertension, diabetes, or CVD are at high risk for CKD,

other high-risk people may be identiﬁed through genetic risk

factors or by varying exposure to environmental pollution,

pesticides, water, and nephrotoxic medications including

signiﬁcant analgesic use and herbal medications, depending

on geographical region. Frameworks in which to consider

speciﬁc regional factors have been offered to facilitate

discussion about the value and context of screening for CKD.

Currently, kidney disease awareness remains low, and

worldwide only 6% of the general population and 10% of the

high-risk population are aware of their CKD status. Impor-

tant to note is that patient advocates with CKD strongly argue

for earlier CKD screening and diagnosis.

They also advocate

for CKD detection to be integrated with patient and family

education and engagement to improve accessing appropriate

healthcare and knowledge and adherence to recommended

lifestyle modiﬁcation and medications.

500

1000

1500

2000

2500

0 10203040 60708090 00105

SDI

DALY rate (per 100,000)

Latin America and Caribbean

Central Europe, eastern Europe, and central Asia

Sub-Saharan Africa

High income

North Africa and Middle East

South Asia Southeast Asia, east Asia, and Oceania

GBD super-region

Figure 2 | Age-standardized chronic kidney disease disability-adjusted life-year (DALY) rates for each location by sociodemographic

index (SDI), both sexes combined, 2019. GBD, global burden of disease. Reproduced from Global Burden of Disease 2019: GBD cause and risk

summaries chronic kidney disease. Lancet. 2020;396:S152–S153.

ª 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article

under the CC BY 4.0 license.

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Use of a simple algorithm such as that shown above in

settings such as primary care, cardiology, and endocrinology

could signiﬁcantly improve the early identiﬁcation and

treatment of CKD (Figure 3).

There are no current evidence-based recommendations

regarding the frequency of screening in people at risk of CKD.

In the setting of diabetes, a consensus report from the Amer-

ican Diabetes Association (ADA) and KDIGO recommends

annual screening of people with diabetes for CKD.

CKD

screening should start at diagnosis of type 2 diabetes (T2D)

because evidence of CKD is often already apparent at this

time. For type 1 diabetes (T1D), screening is recommended

commencing 5 years after diagnosis. The overall costs of a

screening program are largely driven by the frequency of

repeat screening, so the timing of repeated testing should be

guided by CKD risk. There are risk equations available to

estimate the interval risk of developing CKD, and this risk

stratiﬁcation could guide repeat testing intervals.

International considerations

In low- and middle-income regions of the world and in the

lower sociodemographic quintiles, there is a large gap between

CKD burden and provision of adequate healthcare. There is

limited access to kidney replacement therapy (KRT) combined

with the rising prevalence of diabetes and hypertension and

evidence of substantial sex and gender disparities in access to

CKD treatment. These factors highlight the importance of early

identiﬁcation and treatment of risk factors in primary care.

However, the majority of the world’s population with CKD is

in low- and middle-income countries (LMIC) where there are

disparities in access to laboratory diagnostic services, kidney

biopsy, and imaging services, in availability of appropriately

skilled healthcare providers and the availability and afford-

ability of medications. The International Society of Nephrology

survey assessing global kidney healthcare resources reported

that fewer than 1 in 4 surveyed countries had facilities available

for routine measurements of SCr or proteinuria.

Identify adults at risk for CKD

Test for GFR* and ACR ± other markers of kidney damage

†

Test for GFR or ACR if not performed and exclude AKI/AKD

AKI/AKD present:

follow AKI/AKD guidance

GFR <60 ml/min per 1.73 m

and/or

ACR ≥30 mg/g [3 mg/mmol] after 3 months

or earlier if evidence of chronicity

Measure eGFRcr-cys if not

performed and available

CKD not present

Timing of retesting based on

individual characteristics such

as risk of progression

Stage according to GFR and ACR

Establish underlying cause

Estimate risk of progression

Initiate treatment

GFR ≥60 ml/min per 1.73 m

and

ACR <30 mg/g [3 mg/mmol]

and no other markers of

kidney damage present

GFR <60 ml/min per 1.73 m

or ACR ≥30 mg/g [3 mg/mmol]

and/or other markers of kidney damage present

Figure 3 | Screening algorithm for diagnosis and staging of chronic kidney disease (CKD) in adults. Risk factor conditions are listed in

Table 5. *For recommended methods to estimate glomerular ﬁltration rate (eGFR), see Section 1.2.

†

Markers of kidney damage other than

albuminuria may also be used to diagnose CKD, but albumin-to-creatinine ratio (ACR) and GFR are still required to determine stage and

estimate risk of progression. Acute kidney disease (AKD) is deﬁned by the abnormalities of kidney function and/or structure with implications

for health and with a duration of #3 months.

The orange boxes indicate actions in people at risk for CKD and in whom testing should be

performed. The blue boxes indicate testing steps. The green boxes indicate the identiﬁcation of CKD and its stages and the initiation of

treatment. The purple box indicates the identiﬁcation of AKD/acute kidney injury (AKI). Please also see the Kidney Disease: Improving Global

Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury.

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Kidney International (2024) 105 (Suppl 4S), S117–S314 S139

Importantly, slowing CKD progression at early stages

should provide economic beneﬁts and prevent the develop-

ment of kidney failure and cardiovascular complications. A

systematic review of care models in LMIC found that those

supporting primary care providers or allied health workers

achieved effectiveness in slowing GFR decline, as opposed to

interventions centered on specialty care alone.

Where there

are resource limitations, it is logical to deploy resources where

they w ill be most cost-effective, for example, to higher-risk,

preventable stages.

Standardization/accuracy of testing tools including

assays/equipment

The KDIGO 2012 CKD guideline built on recommendations

made to clinical laboratories in the earlier KDOQI 2002

guidance. Clinical laboratories were speciﬁcally charged with

measuring SCr and serum cystatin C using assays with cali-

bration traceable to the international standard reference

materials recommending that, for SCr, there should be

minimal bias compared with isotope-dilution mass spec-

trometry.

Recommendations were also made with respect to

measurement and reporting of albumin and protein in the

urine. Although some of the recommendations have

become part of routine practice, the effective use of clinical

guidelines and therefore effective patient care, including

accurate diagnosis and referral prioritization, clinical

research, and public health prioritization, require

comparability of laboratory results independent of time,

place, and measurement procedure. Key to this is

establishing precision and between-laboratory agreement

with traceability to accepted reference standards wherever

available. Therefore, this guidance document includes

standards for laboratory tests. The International

Consortium for Harmonization of Clinical Laboratory

Results (ICHLR) was established to create a pathway for

harmonization and aid implementation of clinical guidelines

recommending the use of laboratory tests in the diagnosis

and management of disease,

ensuring that both reference

materials and test methodology are harmonized. The

ICHLR aimed to prioritize measurands by medical

importance and both coordinate and stimulate development

of technical and regulatory processes to achieve

harmonization of those measuran ds.

Although this has

been achieved for SCr, the current status of other key

measurands such as cystatin C and urinary albumin is not

yet sufﬁciently clear.

The foundations for this 2024 guideline have been devel-

oped over the last 20 years, galvanizing the collaborative work

of researchers, healthcare providers, laboratory physicians,

patients, and carers. The current updated guideline document

reinforces methods for accurate diagnosis of CKD and pre-

diction, incor porates novel treatment strategies and ap-

proaches to managing people living with CKD, and identiﬁes

further areas for research. Importantly, as the ﬁeld is rapidly

changing, we commit to updating relevant sections of this

document as new evidence becomes available, to ensure more

timely updates than have previously been poss ible.

Adeera Levin, MD, FRCPC

Paul E. Stevens, MB, FRCP

CKD Guideline Co-Chairs

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Kidney International (2024) 105 (Suppl 4S), S117–S314

Special considerations

The Work Group recognizes that kidney diseases affect people

at different times and with different impacts across the whole

lifespan. Thus, enabling a personalized approach, considering

age, sex, and gender for diagnosis, risk assessment, and

treatment is critical. At the extremes of age—the very young

and the very old—diagnostic procedures, treatment aims,

treatment modalities, and decision-making differ due to dif-

ferences in prognosis, treatment options, and prioritization.

In young and middle-aged adults, treatment approaches may

differ due to speciﬁc circumstances, such as pregnancy or

menopause. Sex (biological attributes) and gender (socio-

cultural factors), as well as other important intersectional

factors including but not limited to geographical location,

socioeconomic status (SES), and race and ethnicity, play

important roles in kidney health and disease.

Here we introduce concepts as to why age, sex, and gender

should be considered in the context of diagnosis, treatment,

and care planning in people with CKD. In addition, the

speciﬁc guideline chapters incorporate statements where

special considerations regarding age, sex, and gender are

relevant to clinical practice and understanding.

Considerations in children and adolescents

When the guideline refers to people with CKD, this includes

children (people <10 years old) and adolescents (people

10–19 years old). When there are altered care recommenda-

tions and practice points due to the unique needs of children

or the lack of data to inform recommendations and practice

points, these considerations are discussed w ithin the Pediatric

considerations sections of the guideline.

The management of children and adolescents with CKD

needs special consideration (Figure 4). Children and adults have

different etiologies of CKD. Up to 40%–50% of childhood CKD

is due to congenital anomalies of the kidneys and urinary tract

(CAKUT); the younger the CKD population, the greater the

proportion with CAKUT as the cause.

35,36

CAKUT is

characterized by slower progression to kidney failure and a

higher likelihood of polyuria than the conditions causing CKD

in adults. Pediatric CKD has several unique aspects:

Delivery of care. Pediatric healt hcare providers engage with

not only the person with CKD but also their carers and sib-

lings. Age-appropriate care and education, understood by

both the child and their carers, is necessary. Holistic consid-

eration of the needs and capabilities of the family unit is

important in ensuring effective CKD care. Engage ment with

patients and families must change over the course of child-

hood from being entirely carer-directed for infants, changing

to include the whole family unit in child hood, and then

leaning toward the young person to ensure successful tran-

sition to adult-oriented care.

Child/adolescent

• Growth

• Nutrition

• Weight/BSA-based drug dosing

• Neurocognitive development

• Supporting education

• Transition to adult care

• Holistic approach to care for

the whole family unit

Pregnancy/lactation

• Drug pharmacokinetics

and pharmacodynamics

• Drug teratogenicity

• Risk of CKD progression

• Increased risk of pregnancy

complications, preterm birth

and small for gestational

age babies

• Fertility

Older adults

• Multidimensionality of

chronic conditions/

multimorbidity

• Frailty (including sarcopenia)

• Cognitive function

• Polypharmacy

• Prioritization

• End-of-life care

Gender

• Gender identity

• Gender roles

• Gender relations

• Institutionalized

gender

Sex

• Menopause

• Contraception

of risk factors and

complications

Figure 4 | Special considerations for chronic kidney disease (CKD) care across the lifespan. BSA, body surface area.

www.kidney-international.org special considerations

Kidney International (2024) 105 (Suppl 4S), S117–S314 S141

Growth, puberty, and young adulthood. Childhood and

adolescence are characterized by physical growth and devel-

opment. All CKD care aims to optimize these physiological

processes, which are commonly disrupted by CKD. Puberty is

a time of rapid somatic growth with an increase in muscle

bulk and therefore constitutes a high-risk period for CKD

progression as compromised kidneys may not hypertrophy to

adapt to the larger body size. Adolescence and emerging

adulthood bring individuation and exploration of sexuality

and adult behaviors, and kidney disease care must recognize

and adapt to these changes.

Kidney development and long-term assessment of kidney

risks.

Although nephron formation is complete by 36 weeks of

gestation, kidney function continues to develop throughout

early childhood, with nephron growth and maturatio n pro-

gressing particularly rapidly in the ﬁrst year of life. An actual

increase in GFR over the course of the ﬁrst 1–2 years of life, and

even up to 4 years of age, is expected. A trajectory of increasing

GFR in infancy and very early childhood followed by a period of

relative stability and a subsequent progression in CKD in

adolescence or adulthood is common. Given the long life ex-

pectancy of children, follow-up plans mu st take into account

the risk of late CKD or kidney failure. Healthy children and

adolescents should have excellent kidney function, so an esti-

mated eGFR under 90 ml/min per 1.73 m

(CKD G2–G5)

represents decreased kidney function in these age groups. Early

assessment and intervention of children with CKD is crucial to

maximize overall health across the lifespan.

Neurodevelopment and education. A primary goal of pedi-

atric CKD care is to optimize neurodevelopmental gains.

CKD can affect development, cognition, school attendance,

vocational outcomes, and future employment. Mitigating

these deﬁcits through effective, individualized care is essential

to give children with CKD the best possible future.

Considerations in older adults

Older adults constitute a substantial and steadily growing

proportion of people under nephrology and medical care

globally, especially in Western industrialized countries.

Longevity in many parts of the world is increasing, and thus

the prevalence of CKD in those people is also increasing. The

2022 US Renal Data System (USRDS) annual data report

highlights that the number of individuals initiating KRT is

continuously ascending with increasing age. In Taiwan, for

example, KRT incidence in those aged 75þ was 2858 per

million population (pmp) compared with 1583 pmp among

people aged 65–74 years, 530 pmp among people aged 45 – 64

years, and 97 pmp among people aged 20–44 years. The

pattern is very similar across the g lobe with the majority of

people initiating dialysis over the age of 75, which puts

emphasis on a group of people who are not just old, but very

old, and incorporates more and more people over the age of

80. Octo- and nonagenarians often demonstrate distinct

patterns of disease complexity. These features include multi-

morbidity often accompanied by polypharmacy, frailty,

cognitive impairment, and gerontopsychiatric disorders

among others. Often, several of these features coexist espe-

cially in older adults with CKD.

Implications for agin g adult s with CKD are important in

both diagnosis and treatment. The interpretation of labora-

tory results (speciﬁcally SCr) used in the staging system

should factor in an older adult’s habitus given the frequency

of sarcopenia. A creatinine-based eGFR (eGFRcr) will over-

estimate GFR in the elderly (and others) with sarcopenia

leading to drug overdosing. Urine ACR at the same time will

be falsely high due to the falsely low creatinine in the de-

nominator. Furthermore, the presence of frailty may alter

treatment targets recommended for younger people with

CKD, as they may not necessarily be transferable to older

adults. Strict BP-lowering, for example, may come with the

risk of dizziness, falls, and fractures in older adults, many of

whom are on anticoagulants risking severe hemorrhage.

The multidimensionality of comorbidities in old age poses

challenges, as it demands a sophisticated integrated and

complex multidisciplinary care and treatment approach,

which may not be available in every healthcare system. Life

expectancy in old age is naturally limited compared with

younger people. Perspectives and treatment goals shift over

the life course, and recognizing these in very old adults, as

different from those in middle-aged or younger adults with

CKD, is critical to the development of more personalized care

plans and goals. Speciﬁcally, pure survival may become less of

a priority for an older individual, whereas maintaining an

acceptable, good quality of life (QoL) may be more impor-

tant. The context of a person’s situation and own values and

preferences may modify the prioritizati on for testing, treat-

ment types, and treatment goals. For example, the decision-

making between KRT and conservat ive care should be made

on the basis of the person’s priorities, medical needs, and

informed decision as to beneﬁts and harms of various op-

tions. These informed decisions require good communication

between caregivers, people with CKD, and their relatives/

carers; they require time, “room,” adequate understandable

language, patience, trust, and commitment. Repeated con-

versations are critical, g iven the higher prevalence of cognitive

deﬁcits in older adults with CKD. These cognitive issues

accompany both aging and CKD and frequently remain un-

recognized, thus, impeding shared decision-making and

advance care planning in this group.

In summary, older adults constitute the largest group

among all people with advanced CKD. Although every single

person needs individual care, the multidimensional medical

complexity inherent in very old age is challenging. Where

speciﬁc recommendations or practice points require special

consideration in the elderly, we make clear statements in the

special considerations section and encourage clinicians to

individualize therapies and goals of care in all patients, with

special attention to those of advanced age.

Considerations regarding sex and gender

It is increasingly recognized that sex (biological attributes)

and gender (sociocultural factors) factors across individuals

special considerations www.kidney-international.org

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Kidney International (2024) 105 (Suppl 4S), S117–S314

contribute to differences in kidney health and disease.

37–39

Sex-based variat ion in genetics, physiolog y, immunology, and

anatomy, as well as gender factors such as identity, roles, and

relations in addition to institutionalized gender, inﬂuences

kidney disease pathophysiology, presentation, response to

therapy, complications, and outcomes, highlighting the need

to take these factors into consideration in the care of the

person living with kidney disease.

Globally, the prevalence of CKD not being treated with

dialysis deﬁned by level of eGFR is greater in women than

men.

Progression of CKD has been reported as more rapid

in men,

41,42

in women,

or no difference by sex or gender.

These incongruities are likely a reﬂection of diff erences in

cause of kidney disease and deﬁnitions of outcomes (e.g.,

loss of eGFR or receipt of KRT).

There is substantial literature demonstrating that both sex -

and gend er-related factors (e.g., puberty, menstrual patterns,

hormonal contraception, pregnancy and pregnancy-related

complications, menopause, menopausal hormone therapy,

testosterone levels, and gender-afﬁrming hormone therapy)

play important roles in the risk, progression, complications,

and treatment of kidney disease.

These factors will play prominent roles in progression of

kidney disease across different stages of the life cycle. For

example, the use of some recommended medications has not

been studied in pregnant populations, highlighting the

importance of contraceptive counseling in accordance with a

person’s values and preferences. In other instances, precon-

ception counseling, changing medications to nonteratogenic

options and a multidisciplinary approach, is required to

optimize the outcomes of a potential pregnancy in the setting

of CKD. Sex-based differences in pharmacokinetics and

pharmacodynamics that are accentuated with increasing age

and changing hormonal status may alter the response to

different therapies for the treatment of kidney disease. For

example, women are more likely to report adverse reactions

to angiotensin-converting enzyme inhibitors (ACEi),

which

play a role in adherence and failure to reach guideline-

recommended target doses.

There are differences between women and men in the

detection, recognition, monitoring, referrals, and manage-

ment of CKD.

47,48

Although the reasons behind these

disparities are unclear, access to kidney care may be limited

by familial and other caregiving responsibilities, as well as

ﬁnancial challenges, occupational obligations, and time

constraints, which are inﬂuenced by gender identity (how

an individual self-identiﬁes, behaves, expresses their gender,

and i s perce ived by others, e.g., woman, man, girl, b oy,

and gender-diverse), roles (social expectations and norms

ty pically associated with a g iven gender, e.g., pr imar y

household earner and caregiver), relations (interactions

with and trea tment by ot hers based on an individual’s

perceived and/or expressed gender iden tity), and

institutionalized gender (e.g., distribution of power and

resources in soc iety).

A small but increasing proportion of the world’s popula-

tion identiﬁes as transgender, gender-diverse, or nonbinary

where sex assigned at birth differs from gender identity,

highlighting the urgent need to build transgender cultural

safety within all aspects of kidney disease management and

care.

Taking sex and gender considerations into account is

critical to optimize the care of the individual with kidney

disease. Although there is increasing literature to inform sex-

and gender-speciﬁc recommendations in nephrology, signif-

icant knowledge gaps remain, underscoring the importance of

a person-centered approach in kidney care.

Considerations regarding fertility and pregnancy

Neither fertility nor pregnancy in people w ith CKD was part

of the scope of work for this guideline update, but there will

be special consideration relating to fertility and pregnancy

requiring speciﬁc reference in relevant sections of the

guideline.

Fertility. CKD is associated with decreased female and male

fertility.

50,51

Progressively impaired function of the

hypothalamic-pituitary-gonadal axis appears to play a key

role in the pathophysiology, although multiple factors

contribute to the reduction in fertility in this populati on. In

conjunction with the decreased fertility associated in CKD

and the uncertainty of the impact of assisted reproductive

technologies on kidney function, ongoing discussion of

family planning potential between the person with CKD

and their healthcare provider is essential.

Pregnancy. People with CKD are at risk for adverse preg-

nancy-associated outcomes, including progression of their

underlying CKD, a ﬂare of their kidney disease, and adverse

pregnancy complications including pre-eclampsia, preterm

delivery, and small for gestational age infant.

52,53

The severity

of CKD is associated with risk of adverse pregnancy

outcomes. A multidisciplinary approach to preconception

counseling and man agement of pregnancy is necessary to

achieve optimal outcomes for both the person with CKD

and the infant.

www.kidney-international.org special considerations

Kidney International (2024) 105 (Suppl 4S), S117–S314 S143

Summary of relative and absolute risks relevant to CKD

from meta-analysis of large multinational population

studies in the CKD Prognosis Consortium (CKD-PC)

Outcomes relevant to CKD, and the prognostic importance of

CKD categories

The most highly evaluated endpoints in epidemiological

studies have been all-cause mortality, cardiovascular events

(myocardial infarction, stroke, and heart failure), and kidney-

speciﬁc outcomes (progression to kidney failure and AKI),

although additional outcomes such as all-cause hospitaliza-

tion and incident atrial ﬁbrillation have been studied more

recently. In this section, we highlight newer data derived from

the CKD Prognosis Consor tium (CKD-PC).

We describe

the associations of CKD categories with 10 of these

important outcomes and demonstrate the importance of

different methods of estimating GFR (i.e., using creatinine-

or cystatin C–based equations) on these risk gradients.

Healthcare providers, researchers, and policy makers

should understand the association of CKD parameters (ACR

and eGFR) in populations. The overall distributions of

epidemiolog ical risk across CKD categories on a population

level are presented here. This is not to be confused with the

information presented in Chapter 2, where individualized risk

assessment tools are described, and those tools can be used to

inform clinical and management decisions for individual

people with CKD.

Associations of all complications o f CKD are incre-

mentally increased with worsened categories of estimated

glomerular ﬁltration rate (eGFR) and albuminuria:

updated data.

The KDIGO 2012 Clinical Practice Guideline for the Evalu-

ation and Management of Chronic Kidney Disease introduced

the combined staging by eGFR and albuminuria categories,

which were justiﬁed by their associations with CKD complica-

tions.

The combined associations of eGFR and ACR categories

were presented as “heatmaps,” a color-coded depiction of the

associations of increased risk with worsening CKD, for

outcomes of all-cause mortality, kidney failure, AKI, and

cardiovascular mortality on a population level. In this section,

we provide an update to these CKD heatmaps, which have

been provided by the CKD-PC.

Several changes in the development of these updated

heatmaps are important to highlight.

(i) They now include several clinical databases that allow a

much larger population base, comprising up to 27,503,140

people for the analyses of each adverse outcome.

(ii) The eGFRcr has been changed to the 2021 CKD Epide-

miology Collaboration (CKD-EPI) equation, as this

newer version no longer includes race as a component.

(iii) The number of outcomes has been increased to 10,

including 6 that are cardiovascular related, 2 that are

kidney speciﬁc (kidney failure and AKI), and 2 general

outcomes (all-cause mortality and all-cause

hospitalization).

(iv) Additional analyses have been conducted using the 2021

CKD-EPI combined eGFR equation that incorporates

both creatinine and cystatin C. Although the sample size

for these subsequent analyses is much smaller (n ¼

720,736), it does permit better differentiation of associ-

ations of eGFR and risk and allows validation of CKD

thresholds across populations.

CKD staging by eGFRcr and ACR and association with adverse

events

Figure 5

presents the RRs for all eGFR/ACR combinations

for the 10 identiﬁed outcomes.

The RRs presented have all been adjusted for age, sex,

smoking status (current, former, or never), systolic BP (SBP),

total cholesterol, high-density lipoprotein (HDL) cholesterol,

body mass index (BMI), use of antihypertensive medications,

and a medical history of diabetes, coronary heart disease,

stroke, heart failure, atr ial ﬁbrillation, peripheral artery dis-

ease, cancer, and chronic obstructive pulmonary disease.

Therefore, the RRs can be interpreted as the proportional

elevation in risk for each outcome experienced by people in

that stage of CKD (or non-CKD) compared with people in

the healthiest group. Across all the heatmaps, a consistent

color scheme is used.

The ﬁgures reveal severa l common themes a nd highlig ht

the necessity of having both eGFR and ACR parameters

available in assessing r isk. First, w ithin the CKD popula-

tion,theassociationofriskforall10outcomesincreases

with higher stages of both eGFR and albuminuria. The

ﬁg u res pres e n t only th e RRs for ea c h spe ci ﬁcstageandnot

the absolute risk of experiencing that outcome for people

in the risk cell. This distinction between relative and ab-

solute risks demonstrates the importance of using indi-

vidual risk prediction tools for persons w ith CKD, a subject

of Chapter 2.

Although nearly all CKD categories are at substantially

elevated risk for most outcomes in Figure 5, a distinction must be

made for people in the eGFRcr CKD G3a category and with the

lowest ACR severity (<10 mg/g [<1mg/mmol]).Thisgroupis

portrayed in the lower-risk green color for 7 of the 10 outcomes

presented, although they have 3-fold higher adjusted risk of AKI

and 13-fold higher risk of kidney failure compared with the

reference group. The inconsistent risk association for

populations with CKD G3a, A1, particularly in older adults,

has led to controversy over whether this group should be

relative and absolute risks associated with CKD www.kidney-international.org

S144

Kidney International (2024) 105 (Suppl 4S), S117–S314

considered as having CKD.

The CKD-PC investigators

repeated all 10 heatmaps using creatinine- and cystatin C–

based eGFR (eGFRcr-cys), in part to evaluate whether the

weaker associations of CKD G3a, A1 with clinical outcomes

were caused by the limitations of the speciﬁc creatinine-based

equation eGFRcr, compared with eGFRcr-cys, which has been

established as a better approximation of measured GFR

(mGFR) than eGFRcr (Figure 6

Overall

eGFRcr <10 10–29 30–299 300–999 1000+ <10 10–29 30–299

105+

1.6 2.2 2.9 4.3 5.8 1.1 1.4 2.0

90–104

ref 1.3 1.8 2.6 3.1 ref 1.3 1.6

60–89

1.0 1.3 1.7 2.2 2.8 1.1 1.3 1.6

45–59

1.3 1.6 2.0 2.4 3.1 1.4 1.7 2.0

30–44

1.8 2.0 2.5 3.2 3.9 1.9 2.0 2.4

15–29

2.8 2.8 3.3 4.1 5.6 2.7 3.1 3.1

<15

4.6 5.0 5.3 6.0 7.0 4.6 5.6 4.8

105+

1.4 2.0 3.0 4.1 5.4 1.2 1.6 2.2

90–104

ref 1.3 1.9 2.7 3.6 ref 1.3 1.6

60–89

1.0 1.4 1.7 2.4 3.2 1.1 1.3 1.7

45–59

1.4 1.7 2.2 2.8 3.8 1.4 1.6 1.9

30–44

2.0 2.3 2.8 3.7 4.6 1.6 1.7 2.0

15–29

3.2 3.1 3.5 5.0 6.5 1.8 2.1 2.1

<15

6.1 6.4 6.4 7.3 8.2 3.2 2.8 2.9

105+

0.5 1.2 2.9 7.7 25 1.2 1.7 2.7

90–104

ref 1.8 4.3 12 43 ref 1.3 2.0

60–89

2.3 4.9 10 27 85 1.1 1.4 1.9

45–59

13 19 37 89 236 1.6 1.8 2.4

30–44

50 58 115 240 463 2.2 2.5 3.1

15–29

283 301 443 796 1253 3.6 3.5 4.1

<15

770 1040 1618 2297 2547 5.1 5.7 5.8

105+

1.0 1.6 2.4 3.7 5.5 1.1 1.3 1.7

90–104

ref 1.4 2.1 3.2 5.0 ref 1.2 1.5

60–89

1.6 2.2 3.1 4.3 6.7 1.0 1.2 1.4

45–59

3.5 4.0 5.1 6.9 9.0 1.2 1.3 1.5

30–44

5.6 5.9 6.8 8.6 11 1.4 1.5 1.7

15–29

8.3 8.0 8.5 9.9 10 1.9 1.8 2.0

<15

8.5 11 7.9 5.5 5.7 2.6 2.5 3.1

105+

1.4 1.7 2.1 2.1 2.3 0.9 1.4 1.9

90–104

ref 1.1 1.3 1.5 1.7 ref 1.3 1.9

60–89

1.0 1.1 1.3 1.5 1.8 1.0 1.3 1.8

45–59

1.3 1.3 1.5 1.7 2.1 1.5 1.7 2.1

Urine albumin-creatinine r g/gm ,oitar eninitaerc-nimubla enirUg/gm ,oita

All-cause mortality: 82 cohorts

26 444 384

participants; 2 604 028 events

Myocardial infarction: 64 cohorts

22 838 356 participants; 451 063 events

Kidney failure with replacement therapy: 57 cohorts

25 466 956 participants; 158 846 events

Heart failure: 61 cohorts

24 603 016 participants; 1 132 443 events

Cardiovascular mortality: 76 cohorts

26 022 346 participants; 776 441 events

Stroke: 68 cohorts

24 746 436 participants; 461 785 events

Acute kidney injury: 49 cohorts

23 914 614 participants; 1 408 929 events

22 886 642 participants; 1 068 701 events

Hospitalization: 49 cohorts

25 426 722 participants; 8 398 637 events

Peripheral artery disease: 54 cohorts

24 830 794 participants; 378 924 events

30–44

1.5 1.5 1.6 1.9 2.3 2.0 1.9 2.5

15–29

1.8 1.8 1.9 2.4 2.8 3.3 3.3 3.8

<15

2.7 2.8 3.0 3.2 3.8 9.1 9.0 9.6

300–999 1000+

2.7 3.8

2.2 3.2

2.2 3.1

2.8 3.7

3.2 4.3

4.2 5.1

6.0 6.0

3.1 4.3

2.4 3.1

2.2 3.0

2.3 2.9

2.4 3.0

2.7 3.0

3.2 3.8

4.2 6.9

2.8 4.2

2.7 4.2

3.4 5.0

4.2 6.5

5.8 8.1

7.9 9.9

2.4 3.5

1.9 2.3

1.7 2.2

1.8 2.4

2.0 2.4

2.6 3.0

3.6 4.2

2.8 5.0

2.8 4.3

2.5 3.8

2.9 4.2

3.6 5.0

5.7 8.1

13 14

Figure 5 | Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by creatinine (eGFRcr) and

albumin-to-creatinine ratio (ACR) categories and risks for 10 common complications in multivariable-adjusted analyses. Numbers

reﬂect the adjusted hazard ratio compared with the reference cell. Adjustment variables included age, sex, smoking status (current, former, or

never), systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, body mass index, use of antihypertensive medications,

and a medical history of diabetes, coronary heart disease, stroke, heart failure, atrial ﬁbrillation, peripheral artery disease, cancer, and chronic

obstructive pulmonary disease, where relevant. The colors were determined for each outcome separately using the following rule: the

percentile shaded the darkest green color corresponds to the proportion of cells in the grid without CKD (e.g., 6 of 35 cells with eGFR $60 ml/

min per 1.73 m

and ACR <30 mg/g [<3 mg/mmol]), and the percentile shaded the darkest red color corresponds to proportion expected to be

at highest risk (e.g., 11 of 35 cells with eGFR <15 ml/min per 1.73 m

and albumin-to-creatinine ratio 1000þ mg/g [100þ mg/mmol]). In this

manner, the numbers of green and red cells are consistent across outcomes, but the patterns are allowed to differ. ref, reference cell.

Reproduced with permission from JAMA, Writing Group for the CKD Prognosis Consortium; Grams ME, Coresh J, Matsushita K, et al. Estimated

glomerular ﬁltration rate, albuminuria, and adverse outcomes: an individual-participant data meta-analysis. JAMA. 2023;330(13):1266–1277.

www.kidney-international.org relative and absolute risks associated with CKD

Kidney International (2024) 105 (Suppl 4S), S117–S314 S145

CKD staging by eGFRcr-cys and ACR and risk for adverse

events

Within the CKD-PC collaboration, 720,736 indiv iduals had

measures of blood cystatin C in addition to having eGFRcr

and ACR. The replacement of eGFRcr with eGFRcr-cys in the

heatmap led to several changes in the risk distributions. Most

notably, the groups with eGFR category 45–59 ml/min per

1.73 m

and ACR <10 mg/g [<1 mg/mmol] were moved to

eGFRcr-cys <10 10–29 30–299 300+ <10 10–29 30–299

105+

90–104

60–89

45–59

30–44

<30

105+

90–104

60–89

45–59

30–44

<30

105+

90–104

60–89

45–59

30–44

<30

105+

90–104

60–89

45–59

30–44

<30

105+

90–104

60–89

45–59

Urine albumin-creatinine ratio, mg/g Urine albumin-creatinine ratio, mg/g

All-cause mortality: 11 cohorts

692 802 participants; 97 006 events

Myocardial infarction: 10 cohorts

649 365 participants; 17 926 events

Kidney failure with replacement therapy: 5 cohorts

630 370 participants; 4306 events

Heart failure: 9 cohorts

641 298 participants; 27 406 events

Cardiovascular mortality: 11 cohorts

692 322 participants, 25 322 events

Stroke: 9 cohorts

662 605 participants; 16 909 events

Acute kidney injury: 5 cohorts

630 370 participants; 24 062 events

607 102 participants; 37 278 events

Hospitalization: 3 cohorts

630 489 participants; 464 894 events

Peripheral artery disease: 6 cohorts

642 624 participants; 3943 events

30–44

<30

300+

1.0 1.3 1.6 2.5 0.9 1.2 1.4 2.8

ref 1.3 1.5 2.0 ref 1.2 1.4 1.8

1.2 1.5 1.9 2.5 1.2 1.4 1.5 1.9

1.7 2.2 2.5 3.3 1.6 1.9 2.3 3.3

2.3

2.6

3.4 4.4 2.1 2.6 3.1 3.3

3.6 4.0 5.5 7.1 5.1 3.0 4.9 5.0

1.0 1.4 1.8 4.1 1.0 1.2 1.6 2.5

ref 1.5 1.6 2.9 ref 1.2 1.5 2.3

1.2 1.7 2.3 3.4 1.2 1.4 1.8 2.5

1.9 2.7 3.2 4.6 1.6 1.7 2.1 2.7

2.5 3.5 4.5 5.9 1.7 2.0 2.3 2.6

5.8 5.0 6.1 8.7 1.9 2.3 2.8 4.4

0.6 0.8 2.3 10 0.9 1.2 1.7 3.7

ref 1.5 4.5 11 ref 1.3 1.4 2.5

1.9 3.7 8.3 31 1.2 1.6 1.9 3.0

5.8 13 25 73 1.5 2.2 3.0 4.1

20 23 78 191 2.5 2.9 4.1 5.7

111 261 343 580 5.3 4.8 6.5 7.7

0.8

1.0

1.4 3.5 0.9 1.0 1.1 1.9

ref 1.3 1.7 2.8 ref 1.2 1.4 2.2

1.6 2.5 2.9 5.3 1.1 1.3 1.5 2.0

3.9 4.7 5.5 7.5 1.3 1.6 1.8 2.2

5.8 7.0 8.4 10 1.6 2.0 2.2 2.5

11 12 12 21 2.0 2.0 2.7 4.4

1.0 1.1 1.1 1.6 0.9 1.9 1.8 2.9

ref 1.1 1.3 1.4 ref 1.5 2.0 3.2

1.1 1.2 1.3 1.6 1.3 1.8 2.1 3.9

1.3 1.4 1.5 1.7 2.5 3.7 3.3 4.0

1.5 1.5 1.6 2.1 4.0 3.7 4.5 6.9

1.8 2.0 2.1 3.0 7.8 4.5 9.0 12

Figure 6 | Associations of chronic kidney disease (CKD) staging by estimated glomerular ﬁltration rate by creatinine and cystatin C

(eGFRcr-cys) and albumin-to-creatinine ratio categories and risks for 10 common complications in multivariable-adjusted analyses.

Numbers reﬂect the adjusted hazard ratio compared with the reference cell. Adjustment variables included age, sex, smoking status (current,

former, or never), systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, body mass index, use of antihypertensive

medications, and a medical history of diabetes, coronary heart disease, stroke, heart failure, atrial ﬁbrillation, peripheral artery disease, cancer,

and chronic obstructive pulmonary disease, where relevant. The colors were determined for each outcome separately using the following rule:

the percentile shaded the darkest green color corresponds to the proportion of cells in the grid without CKD (e.g., 6 of 24 cells), and the

percentile shaded the darkest red color corresponds to proportion expected to be at highest risk (e.g., 5 of 24 cells). In this manner, the numbers

of green and red cells are consistent across outcomes, but the patterns are allowed to differ. ref, reference cell. Reproduced with permission

from JAMA, Writing Group for the CKD Prognosis Consortium; Grams ME, Coresh J, Matsushita K, et al. Estimated glomerular ﬁltration rate,

albuminuria, and adverse outcomes: an individual-participant data meta-analysis. JAMA. 2023;330(13):1266–1277.

relative and absolute risks associated with CKD www.kidney-international.org

S146

Kidney International (2024) 105 (Suppl 4S), S117–S314

higher risk for all 10 outcomes, and this cell was no longer

labeled green for any of the complications (Figure 6). The

distinction in the se risk relationships was further explored

using spline analyses to depict the risk relationships of

eGFRcr and eGFRcr-cys with all the 10 complications. For

the 8 outcomes that are not inﬂuenced by changes in

creatinine (all except kidney failure and AKI), eGFRcr

exhibited a J-shaped association such that risk increased

with eGFR values over 105 ml/min per 1.73 m

(Figure 7

). In contrast, eGFRcr-cys demonstrated much

more linear associations with each of these complications

throughout its distribution.

Based upon the risk relationships of eGFRcr-cys and

ACR categories with all complications, the existing CKD

staging is appropriate among both younger and older

adults.

Some authors have suggested that the GFR threshold for

CKD of 60 ml/min per 1.73 m

should be raised to 75 ml/min

per 1.73 m

for younger adults and lowered to 45 ml/min per

1.73 m

for older adults.

In younger adults, the purpose of a

higher GFR threshold reﬂects the longer risk horizon for

younger people, which could lead to higher lifetime CKD

progression risks for a given GFR stage. However, the

higher lifetime progression risks in younger adults with

GFR 60–89 ml/min per 1.73 m

can be addressed in their

management without changing the deﬁnition of CKD.

Efforts should be directed at people with higher risk with

GFR levels >60 ml/min per 1.73 m

to prevent the

incidence of CKD or further reductions in GFR.

Among older adults, the ﬁndings of consistently elevated

RR for older adults with CKD G3a, A1, as deﬁned by eGFRcr-

cys, support the inclusion of this large group in the CKD

population. These elevated RRs tell us how much more likely

the outcome is compared with the reference group (eGFR 90–

104 ml/min per 1.73 m

and ACR <10 mg/g [<1 mg/

mmol]). Crucially, they do not tell us what the overall like-

lihood of the outcome, the absolute risk, is. The absolute risk

for important CKD complications is higher among older than

younger adults at nearly every stage, particularly for CVD,

heart failure, and mortalit y. Therefore, this population is also

likely to beneﬁt from having their CKD diagnosed, staged,

and treated.

Rationale for using cystatin C containing equations for CKD

staging

The rationale for using cystatin C versus SCr, or a combi-

nation of both, in eGFR equations is that creatinine, which is

directly linked to muscle mass, may be misleading at extremes

of body habitus, or in speciﬁc conditions (spinal cord injuries

and sarcopenia), and that cystatin C is impacted by different

variables (steroid use, thyroid disease, and cancer). Thus,

because neither is a perfect marker to use for estimating

0.7

1.5

Hazard ratio

0.7

1.5

Hazard ratio

15 30 45 60 75 90 105 120

eGFRcr, ml/min/1.73 m

eGFRcr-cys, ml/min/1.73 m

15 30 45 60 75 90 105 120

All-cause mortality, 721394 participants; 102 910 events

Cardiovascular mortality, 719987 participants; 27 051 events

All-cause hospitalization, 676 519 participants; 7862 events

Myocardial infarction, 711 478 participants; 18 659 events

Stroke, 711293 participants; 17 609 events

Heart failure, 674 255 participants; 28 530 events

Peripheral artery disease, 660 412 participants; 4458 events

Kidney failure with replacement therapy, 637 387 participants; 24 342 events

Acute kidney injury, 632 452 participants; 466 201 events

Figure 7 | Hazard ratios for adverse outcomes using the continuous model of estimated glomerular ﬁltration rate (eGFR), comparison

of the shape of associations between creatinine-based eGFR (eGFRcr) and creatinine and cystatin C–based eGFR (eGFRcr-cys) in the

population with cystatin C (eGFRcr-cys population). (a) Associations of eGFR based on creatinine alone with all-cause mortality,

cardiovascular mortality, all-cause hospitalizations, myocardial infarction, stroke, heart failure, atrial ﬁbrillation, and peripheral artery disease; (b)

Associations of eGFR based on creatinine and cystatin C with all-cause mortality, cardiovascular mortality, all-cause hospitalizations, myocardial

infarction, stroke, heart failure, atrial ﬁbrillation, and peripheral artery disease. Reproduced with permission from JAMA, Writing Group for the

CKD Prognosis Consortium; Grams ME, Coresh J, Matsushita K, et al. Estimated glomerular ﬁltration rate, albuminuria, and adverse outcomes: an

individual-participant data meta-analysis. JAMA. 2023;330(13):1266–1277.

www.kidney-international.org relative and absolute risks associated with CKD

Kidney International (2024) 105 (Suppl 4S), S117–S314 S147

clearance, the combination of the 2 compounds gives more

accurate estimates of GFR when compared with measured

values.

Very low levels of SCr often represent poor health status,

such as frailty or sarcopenia, which limits the production of

creatinine. This biological feature of creatinine (i.e., relation

to muscle mass) has limited its prognostic utility and results

in reducing the risk associations for eGFRcr 45– 60 ml/min

per 1.73 m

and elevating risks for eGFRcr >110 ml/min per

1.73 m

. These limitations are not observed when risk is

estimated using eGFRcr-cys or cystatin C–based eGFR

(eGFRcys) (Figure 7).

When comparing GFR estimates using these 2 ﬁltration

markers, risk gradients are consistently stronger for most

outcomes for eGFRcys in comparison with eGFRcr. Therefore,

for the purpose of evaluating the association of eGFR with

outcomes (i.e., projecting prognosis for people with CKD), the

eGFRcys or eGFRcr-cys can be considered more accurate.

relative and absolute risks associated with CKD www.kidney-international.org

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Kidney International (2024) 105 (Suppl 4S), S117–S314

Summary of recommendation statements and practice

points

Chapter 1: Evaluation of CKD

1.1 Detection and evaluation of CKD

1.1.1 Detection of CKD

Practice Point 1.1.1.1: Test people at risk for and with chronic kidney disease (CKD) using both urine albumin mea-

surement and assessment of glomerular ﬁltration rate (GFR).

Practice Point 1.1.1.2: Following incidental detection of elevated urinary albumin-to-creatinine ratio (ACR), hematuria,

or low estimated GFR (eGFR), repeat tests to conﬁrm presence of CKD.

1.1.2 Methods for staging of CKD

Recommendation 1.1.2.1: In adults at risk for CKD, we recommend using creatinine-based estimated glomer-

ular ﬁltration rate (eGFRcr). If cystatin C is available, the GFR category should be

estimated from the combination of creatinine and cystatin C (creatinine and cystatin

C–based estimated glomerular ﬁ ltration rate [eGFRcr-cys]) (1B).

1.1.3 Evaluation of chronicity

Practice Point 1.1.3.1: Proof of chron icity (duration of a minimum of 3 months) can be established by:

(i) review of past measurements/estimations of GFR;

(ii) review of past measurements of albuminuria or proteinuria and urine microscopic

examinations;

(iii) imaging ﬁndings such as reduced kidney size and reduction in cortical thickness;

(iv) kidney pathological ﬁndings such as ﬁbrosis and atrophy;

(v) medical history, especially condit ions known to cause or contribute to CKD;

(vi) repeat measurements within and beyond the 3-month point.

Practice Point 1.1.3.2: Do not assume chronicity based upon a single abnormal level for eGFR and ACR, as the ﬁnding

could be the result of a recent acute kidney injury (AKI) event or acute kidney disease (AKD).

Practice Point 1.1.3.3: Consider initiation of treatments for CKD at ﬁrst presentation of decrea sed GFR or elevated ACR

if CKD is deemed likely due to presence o f other clinical indicators.

1.1.4 Evaluation of cause

Practice Point 1.1.4. 1: Establish the cause of CKD using clinical context, personal and family history, social and envi-

ronmental factors, medications, physical examination, laboratory measures, im aging, and genetic

and pathologic diagnosis (Figure 8).

www.kidney-international.org summary of recommendation statements and practice points

Kidney International (2024) 105 (Suppl 4S), S117–S314 S149

Practice Point 1.1.4.2: Use tests to establish a cause based on resources available (Table 6

22,98-100

Recommendation 1.1.4.1: We suggest performing a kidney biopsy as an acceptable, safe, diagnostic test to

evaluate cause and guide treatme nt decisions when clinically appropriate (2D).

1.2 Evaluation of GFR

1.2.1 Other functions of kidneys besides GFR

Practice Point 1.2.1.1: Use the term “GFR” when referring to the speciﬁc kidney function of glomerular ﬁltration. Use the

more general term “kidney function(s)” when dealing with the totality of functions of the kidney.

Physical

exam

Nephrotoxic

medications

Symptoms and signs

of urinary tract

abnormalities

Symptoms and signs

of systemic diseases

Laboratory tests, imaging, and tissue sample, such as:

• Urinalysis and urine sediment

• Urine albumin-to-creatinine ratio

• Serologic tests

• Ultrasound

• Kidney biopsy

• Genetic testing

Medical

history

Social and

environmental

history

Obtain careful family history

for possible genetic causes,

including family pedigree for CKD

Figure 8 | Evaluation of cause of chronic kidney disease (CKD).

Table 6 | Guidance for the selection of additional tests for evaluation of cause

Test category Examples Comment or key references

Imaging Ultrasound, intravenous urography, CT kidneys

ureters bladder, nuclear medicine studies, MRI

Assess kidney structure (i.e., kidney shape, size, symmetry, and evidence of

obstruction) for cystic disease and reﬂux disease.

Evolving role of additional technologies (e.g., 3D ultrasound)

Kidney biopsy Ultrasound-guided percutaneous Usually examined by light microscopy, immunoﬂuorescence, and electron

microscopy, and, in some situations, may include molecular diagnostics

Used for exact diagnosis, planning treatment, assessing activity and

chronicity of disease, and likelihood of treatment response; may also be

used to assess genetic disease

Laboratory tests:

serologic, urine

tests

Chemistry including acid-base and electrolytes,

serologic tests such as anti-PLA2R, ANCA, anti-GBM

antibodies

Serum-free light chains, serum, and urine protein

electrophoresis/immunoﬁxation

Urinalysis and urine sediment examination

Refer to KDIGO 2021 Clinical Practice Guideline for the Management of

Glomerular Diseases

Increasing recognition of the role of light chains in kidney disease even in

the absence of multiple myeloma (monoclonal gammopathy of renal

signiﬁcance [MGRS])

Presence of persistent hematuria or albuminuria is critical in determining

differential diagnosis

Genetic testing APOL1, COL4A3, COL4A4, COL4A5, NPHS1, UMOD,

HNF1B, PKD1, PKD2

Evolving as a tool for diagnosis, increased utilization is expected.

Recognition that genetic causes are more common and may present

without classic family history

99,100

ANCA, antineutrophil cytoplasmic antibody; APOL1, apolipoprotein 1; COL4A, type IV collagen alpha chain; CT, computed tomography; GBM, glomerular basement membrane;

HNF1B, hepatocyte nuclear factor 1B; MRI, magnetic resonance imaging; NPHS1, congenital nephrotic syndrome; PKD1, polycystic kidney disease-1; PKD2, polycystic kidney

disease-2; PLA2R, M-type phospholipase A2 receptor; UMOD, uromodulin.

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1.2.2 Guidance to physicians and other healthcare providers

Practice Point 1.2.2.1: Use serum creatinine (SCr) and an estimating equation for initial assessment of GFR (Figure 11).

Recommendation 1.2.2.1: We recommend using eGFRcr-cys in clinical situations when eGFRcr is less accurate

and GFR affects clinical decision-making (Table 8

127-142

) (1C).

Practice Point 1.2.2.2: Where more accurate ascertainment of GFR will impact treatment decisions, measure GFR using

plasma or urinary clearance of an exogenous ﬁltration marker (Table 9).

Practice Poi nt 1.2.2.3: Understand the value and limitations in both eGFR and measured glomerular ﬁltration rate (mGFR)

as well as the variability and factors that inﬂuence SCr and cystatin C measurements.

Practice Point 1.2.2.4: Interpretation of SCr level requires consideration of dietary intake.

Initial test – eGFRcr*

Consider sources of error and need for

more accurate assessment.

Is eGFR thought to be accurate?

Consider potential sources of error in eGFRcr-cys

and need for an even more accurate assessment.

†

Is a more accurate assessment needed?

NoYes

No Yes

Measure

cystatin C

Evaluation of GFR for clinical application

15 30 45 60 90 120

Use eGFRcr

Measure

GFR

Use

GFRcr-cys

‡

Figure 11 | Approach to glomerular ﬁltration rate (GFR) evaluation using initial and supportive tests. The algorithm describes the

approach to the evaluation of GFR. The approach uses initial and supportive testing to develop a ﬁnal assessment of true GFR and to apply it in

individual decision-making. The initial test for the evaluation of GFR is creatinine-based estimated GFR (eGFRcr), which will be available for most

people because creatinine is measured routinely as part of the basic metabolic panel. If eGFRcr is expected to be inaccurate, or if a more

accurate assessment of GFR is needed for clinical decision-making, such as diagnosis or staging of chronic kidney disease or drug dosing, then,

if available, cystatin C should be measured, and creatinine and cystatin C–based estimated GFR (eGFRcr-cys) should be estimated. If eGFRcr-cys

is expected to be inaccurate, or if an even more accurate assessment of GFR is needed for clinical decision-making, then, if available, GFR should

be measured using plasma or urinary clearance of exogenous ﬁltration markers. *Initial test may be estimated GFR by cystatin C (eGFRcys or

eGFRcr-cys) in otherwise healthy populations with changes in creatinine generation due to non-GFR determinants such as changes in muscle

mass or creatinine secretion or extrarenal elimination due to the use of speciﬁc medications.

†

Sources of error in eGFRcr-cys include very low

muscle mass or very high levels of inﬂammation, high catabolic states, or exogenous steroid use.

‡

Consider eGFRcys rather than eGFRcr-cys in

otherwise healthy populations with decreased creatinine generation due to reduced muscle mass or decreased creatinine secretion or

extrarenal elimination due to the use of speciﬁc medications.

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Table 8 | Indications for use of cystatin C

Domain Speciﬁc clinical condition Cause of decreased accuracy Comments on GFR evaluation

Body habitus and changes

in muscle mass

Eating disorders

127

Non-GFR determinants of SCr eGFRcys may be appropriate if no comorbid illness

other than reduction in muscle mass.

Extreme sport/exercise/

body builder

Non-GFR determinants of SCr eGFRcys may be appropriate if an increase in muscle

mass is the only abnormality.

Above-knee amputation

128

Non-GFR determinants of SCr eGFRcys may be appropriate in those without other

comorbid conditions. Suggest eGFRcr-cys in

those with comorbid illness.

Spinal cord injury with

paraplegia/paraparesis or

quadriplegia/quadriparesis

Non-GFR determinants of SCr eGFRcys may be appropriate in those without other

comorbid illness. Suggest eGFRcr-cys in those

with comorbid illness.

Class III obesity

a,b

Non-GFR determinants of SCr

and SCys

eGFRcr-cys demonstrated to be most accurate.

Lifestyle Smoking

129-131

Non-GFR determinants of SCys Minimal data, suggest eGFRcr if no changes to non-

GFR determinants of SCr or comorbid illness.

Diet Low-protein diet Non-GFR determinants of SCr

Minimal data, suggest eGFRcr may be appropriate if

no changes to non-GFR determinants of SCr or no

comorbid illness.

Keto diets Non-GFR determinants of SCr

Vegetarian Non-GFR determinants of SCr

High-protein diets

and creatine supplements

Non-GFR determinants of SCr

Illness other than CKD Malnutrition Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

eGFRcr-cys may be less accurate because of

coexistence of malnutrition and inﬂammation.

Suggest using mGFR for treatment decisions

based on the level of GFR.

Cancer

a,132-137

Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

eGFRcr-cys demonstrated to be most accurate in

populations studied but likelihood of lesser

accuracy in more frail people or in cancers with

high cell turnover. Suggest using mGFR for

treatment decisions based on the level of GFR.

Heart failure

a,138,139

Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

Although limited data, eGFRcys appears less biased

but all have low accuracy. Suggest using eGFRcr-

cys or eGFRcys for routine GFR evaluation. Suggest

using mGFR for treatment decisions based on the

level of GFR.

Cirrhosis

a,79,140,141

Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

Although limited data, eGFRcys appears less biased

but all have low accuracy. Suggest using eGFRcr-

cys or eGFRcys for routine GFR evaluation. Suggest

using mGFR for treatment decisions based on the

level of GFR.

Catabolic consuming

diseases

Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

Minimal data but eGFRcr-cys may be inaccurate.

Suggest using eGFRcr-cys vs. eGFRcr for routine

GFR evaluation. Suggest using mGFR for treatment

decisions based on the level of GFR.

Muscle wasting diseases

142

Chronic illness, presumed

impact on non-GFR

determinants of SCr and SCys

Minimal data. One study shows large bias for both

eGFRcr and eGFRcys. Suggest using eGFRcr-cys

for routine GFR evaluation. Suggest using mGFR

for treatment decisions based on the level of GFR.

Medication effects Steroids (anabolic, hormone) Non-GFR determinants of SCr.

Effect on SCys not known

Physiological effect on SCys unknown, suggest

eGFRcr-cys.

Decreases in tubular secretion Non-GFR determinants of SCr eGFRcys may be appropriate if medication affects only

creatinine and no comorbid illness. Suggest using

mGFR for treatment decisions based on the level

of GFR.

Broad spectrum antibiotics

that decrease extrarenal

elimination

Non-GFR determinants of SCr eGFRcys may be appropriate if medication affects only

creatinine and no comorbid illness. Suggest using

mGFR for treatment decisions based on the level

of GFR.

eGFR, estimated glomerular ﬁltration rate; eGFRcr, creatinine-based estimated GFR; eGFRcr-cys, creatinine and cystatin C–based estimated GFR; GFR, glomerular ﬁltration rate;

mGFR, measured glomerular ﬁltration rate; SCr, serum creatinine; SCys, serum cystatin C.

Data summarized in Adingwupu et al.

149

Obesity class III varies by region but commonly body mass index >40 or >35 kg/m

Catabolic consuming disease may include tuberculosis, AIDS, hematologic malignancies, and severe skin diseases. There are no data with measured glomerular ﬁltration rate

(mGFR) to evaluate this directly.

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Practice Point 1.2.2.5: Assess the potential for error in eGFR when assessing a change in GFR over time.

Practice Point 1.2.2.6: Consider the use of cystatin C–based estimated glomerular ﬁltration rate (eGFRcys) in some speciﬁc

circumstances.

Practice Point 1.2.2.7: Understand the implications of differences between eGFRcr and eGFRcys, as these may be infor-

mative, in both direction and magnitude of those differences.

Practice Point 1.2.2.8: Consider timed urine collections for measured creatini ne clearance if mGFR is not available and

eGFRcr-cys is thought to be inaccurate.

1.2.3 Guidance to clinical laboratories

Practice Point 1.2.3.1: Implement the laboratory standards of care outlined in Table 11 to ensure accuracy and reliability

when assessing GFR using creatinine and cystatin C.

Practice Point 1.2.3.2: Given available reso urces, clinical laboratories may consider the possibility of measurement of both

creatinine and cystatin either as an in-house test or as a referred test.

Special considerations

Pediatric considerations.

Practice Point 1.2.3.3: Laboratories measuring creatinine in infants or small children must ensure their quality control

process include the lowest end of the expected range of values for the group of interest.

Practice Point 1.2.3.4: Consider the consistent use of enzymatic creatinine assays in children, given the hig her relat ive

contribution of non-creatinine chromogens to measured creatinine in children when using the

Jaffe assay, and the high prevalence of icteri c and hemolyzed samples in the neonatal period.

Practice Point 1.2.3.5: An eGFRcr level <90 ml/min per 1.73 m

can be ﬂagged as “low” in children and adolescents over the

age of 2 years.

Table 9 | Comparison of estimated GFR and measured GFR

Estimated GFR by SCr and/or cystatin C Measured GFR

Inexpensive and easy to implement More expensive, more time-consuming, and invasive

Widely available and may also be used

at point of care, easily repeatable

Only available in certain centers

Methods to measure that do not require urine collections are available (i.e., plasma clearance)

Most protocols require repeat blood samples potentially over a long duration

Microsampling tests by ﬁngerpick enable point-of-care testing. Testing has been described,

but not routinely performed

Not sufﬁciently accurate and precise

for all clinical situations

Accurate for GFR in all situations and across the GFR range. Requires individualized protocols

Lags behind changes in GFR Able to identify early changes in GFR

Subject to non-GFR determinant confounding Less inﬂuenced by non-GFR determinants

GFR, glomerular ﬁltration rate; SCr, serum creatinine.

Table 11 | Implementation standards to ensure accuracy and reliability of GFR assessments using creatinine and cystatin C

 Report eGFR in addition to the serum concentrations of ﬁltration markers using validated equations.

 Report eGFR rounded to the nearest whole number and relative to a body surface area (BSA) of 1.73 m

in adults using the units ml/min per 1.73 m

 Reported eGFR levels <60 ml/min per 1.73 m

should be ﬂagged as being low.

 When reporting levels of ﬁltration markers, report:

(i) SCr concentration rounded to the nearest whole number when expressed as standard international units (

mol/l) and rounded to the nearest

100th of a whole number when expressed as conventional units (mg/dl);

(ii) serum cystatin C concentration rounded to the nearest 100th of a whole number when expressed as conventional units (mg/l).

 Measure ﬁltration markers using a speciﬁc, precise (coefﬁcient of variation [CV] <2.3% for creatinine and <2.0% for cystatin C) assay with calibration

traceable to the international standard reference materials and desirable bias (<3.7% for creatinine and <3.2% for cystatin C) compared with reference

methodology (or appropriate international standard reference method group target in external quality assessment [EQA] for cystatin C).

 Use an enzymatic method to assay creatinine, where possible.

 Separate serum/plasma from red blood cells by centrifugation within 12 hours of venipuncture.

 When cystatin C is measured, measure creatinine on the same sample to enable calculation of eGFRcr-cys.

eGFR, estimated glomerular ﬁltration rate; eGFRcr-cys, estimated glomerular ﬁltration rate based on creatinine and cystatin C; GFR, glomerular ﬁltration rate; SCr, serum

creatinine.

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1.2.4 Selection of GFR estimating equations

Recommendation 1.2.4.1: We recommend using a validated GFR estimating equation to derive GFR from serum

ﬁltration markers (eGFR) rather than relying on the serum ﬁltration markers alone (1D).

Practice Point 1.2.4.1: Use the same equation within geographical regions (as deﬁned locally [e.g., continent, country,

region] and as large as possible). Within such regions, equations may differ for adults and children.

Practice Point 1.2.4.2: Use of race in the computation of eGFR should be avoided.

Special considerations

Pediatric considerations.

Practice Point 1.2.4.3: Estimate GFR in children using validated equat ions that have been developed or validated in

comparable populations.

1.3 Evaluation of albuminuria

1.3.1 Guidance for physicians and other healthcare providers

Practice Point 1.3.1.1: Use the following measurements for initial testing of albuminuria (in descending order of pref-

erence). In all cases, a ﬁrst void in the mo rning midstream sample is preferred in adults and

children.

(i) urine ACR, or

(ii) reagent strip urinalysis for albumin and ACR with automated reading.

If measuring urine protein, use the following measurements:

(i) urine protein-to-creatinine ratio (PCR),

(ii) reagent strip urinalysis for total protein with automated reading, or

(iii) reagent strip urinalysis for total protein with manual reading.

Practice Point 1.3.1.2: Use more accurate methods when albuminuria is detected using less accurate methods.

 Conﬁrm reagent strip positive albuminuria and/or proteinuria by quantitative laborat ory mea-

surement and express as a ratio to urine creatinine wherever possible (i.e., quantify the ACR or

PCR if initial semiquantitative tests are positive).

 Conﬁrm ACR ‡30 mg/g (‡3 mg/mmol) on a random untimed urine with a subsequent ﬁrst

morning void in the morning midstream urine sample.

Practice Point 1.3.1.3: Understand factors that may affect interpretation of measurements of urine albumin and urine

creatinine and order conﬁrmatory tests as indicated (Table 16).

Table 16 | Factors causing biological variation in urine albumin or urine protein

Factor Falsely elevated ACR or PCR False decrease in ACR or PCR

Variability in urine

albumin or protein

Hematuria Increases albumin and protein in the urine

Menstruation Increases albumin and protein in the urine

Exercise

259

Increases albumin and protein in the urine

Infection

260,261

Symptomatic urinary infection can cause

production of protein from the organism

Nonalbumin proteins Other proteins may be missed by albumin reagent strips

Variability in urinary

creatinine concentration

Biological sex Females have lower urinary creatinine excretion,

therefore higher ACR and PCR

Males have higher urinary creatinine excretion,

therefore lower ACR and PCR

Weight

73,160

Low urinary creatinine excretion consistent with low

weight can cause high ACR or PCR relative to

timed excretion

High urinary creatinine excretion consistent with high weight

can cause low ACR or PCR relative to timed excretion

Changes in creatinine

excretion

Lower urinary creatinine excretion with AKI

or low-protein intake

High urinary creatinine excretion with high-protein intake

or exercise

ACR, albumin-to-creatinine ratio; AKI, acute kidney injury; PCR, protein-to-creatinine ratio.

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Special considerations

Pediatric considerations.

Practice Point 1.3.1.4: In children, obtain a ﬁrst morning urine sample for initial testing of albuminuria and proteinuria

(in descending order of preference):

(i) Both urine PCR and urine ACR,

(ii) Reagent strip urinalysis for total protein and for albumin with automated reading, or

(iii) Reagent strip urinalysis for total protein and for albumin with manual reading.

1.3.2 Guidance to clinical laboratories

Practice Point 1.3.2.1: Implement the laboratory reporting and handling standards outlined in Table 17 to ensure accuracy

and reliability of the ﬁndings when assessing urine samples.

Practice Point 1.3.2.2: Implementation of an external quality assessment scheme/program for urine albumin and creati-

nine, including calculation of the ACR, is a preferred practice for laboratories.

1.4 Point-of-care testing

Recommendation 1.4.1: We suggest that point-of-care testing (POCT) may be used for creatinine and urine

albumin measurement whe re access to a labora tory is limited or providing a test at the

point-of-care facilitates the clinical pathway (2C).

Practice Point 1.4.1: Whenever a POCT device is used for creatinine and urine albumin testing, ensure that the same pre-

analytical, analytical, and postanalytical quality criteria relating to the specimen collection and perfor-

mance of the device, including external quality assessment, and the interpretation of the result is used.

Practice P oint 1.4.2: Where a POCT device for creatinine testing is being used, generate an estimate of GFR. Use the

equation consistent with that used within the region.

P ractice Point 1.4.3: Where a POCT device is being used for albuminuria testing, the capability of also analyzing

creatinine and producing an ACR is important. Assess the ability of the POCT ACR devices to

produce a positive result in 85% of people with signiﬁcant albuminuria (ACR ‡30 mg/g or ‡3 mg/

mmol), as part of the evaluation and consideration of using the device.

Chapter 2: Risk assessment in people with CKD

2.1 Overview on monitoring for progression of CKD based upon GFR and ACR categories

Practice Point 2.1.1: Assess albuminuria in adults, or albuminuria/proteinuria in children, and GFR at least annually in

people with CKD.

Practice Point 2.1.2: Assess albuminuria and GFR more o ften for individuals at higher risk of CKD progression

when measurement will impact therapeutic decisions.

Practice Point 2.1.3: For people with CKD, a change in eGFR of >20% on a subsequent test exceeds the expected

variability a nd warrants evaluation.

Practice Point 2.1.4: Among people with CKD who initiate hemodyna mically active therapies, GFR reductions of

>30% on subsequent testing exceed the expected variability and warrant evaluation.

Practi ce Point 2.1.5: For albuminuria monitoring of people with CKD, a doubling of the ACR on a subsequent test

exceeds laboratory variability and warrants evaluation.

Table 17 | Implementation standards to ensure accuracy and reliability of urine samples

 Samples for albumin measurement analyzed fresh or stored at 4



C for up to 7 days

 Samples for albumin measurement should not be stored frozen at 20



 Report ACR in untimed urine samples in addition to urine albumin concentration rather than the concentrations alone

 Reporting to 1 decimal place for ACR whether mg/mmol or mg/g

 Analytical CV of methods to measure urine albumin should be <15%.

ACR, albumin-to-creatinine ratio; CV, coefﬁcient of variation.

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2.2 Risk prediction in people with CKD

Recommendation 2.2.1: In people with CKD G3–G5, we recommend using an externally validated risk equation

to estimate the absolute risk of kidney failure (1A).

Practi ce Point 2.2.1: A 5-year kidney failure risk of 3%–5% can be used to determine need for nephrology referral in

addition to criteria based on eGFR or urine ACR, and other clinical considerations.

Practice Point 2.2.2: A 2-year kidney failure risk of >10% can be used to determine the timing of multidisciplinary care

in addition to eGFR-based criteria and other clinical considerations.

Practi ce Poin t 2.2.3: A 2-year kidney failure risk threshold of >40% can be used to determine the modality education,

timing of preparation for kidney replacement therapy (KRT) including vascular access planning or

referral for transplantation, in addition to eGFR-based criteria and other clinical considerations.

Pra ctic e P o int 2. 2 . 4 : Note that risk prediction equations developed for use in people with CKD G3–G5, may not

be valid for use in those with CKD G1–G2.

Practi ce Point 2. 2.5: Use disease-speciﬁc, externally validated prediction equations in people with immunoglobulin

A nephropathy (IgAN) and autosomal dominant polycystic kidney disease (ADPKD).

2.3 Prediction of cardiovascular risk in people with CKD

Practice Point 2.3.1: For cardiovascular risk prediction to guide preventive therapies in people with CKD, use

externally validated models that a re either developed within CKD populations or that incor-

porate eGFR and albuminuria.

Prac ti ce Poi nt 2.3.2 : For mortality risk prediction to guide discussions about goals of care, use externally validated

models that predict all-cause mortality speciﬁcally developed in the CKD population.

Chapter 3: Delaying CKD progression and managing its complications

3.1 CKD treatment and risk modiﬁcation

Practice Point 3.1.1: Treat people with CKD with a comprehensive treatment strategy to reduce risks of progression of

CKD and its associated complications (Figure 17).

3.2 Lifestyle factors

Practice Point 3.2.1: Encourage people with CKD to undertake physical activity compatible with cardiovascular

health, tol erance, a nd level of f railty; achieve an optimal body mass index (BMI); a nd not to use

tobacco products. Referral to provider s and programs (e.g., psycholo gists, rena l dietitians or

accredited nutrition providers, pharmacists, physical and occupational therapy, and smoking

cessation programs) should be offered where indicated and available.

3.2.1 Avoiding use of tobacco products

[No speciﬁc recommendations or practice points]

Impact on CKD pathophysiology

CKD manifestations

Prevention and treatment of clinical

symptoms and signs (including blood pressure)

Maximize health-related quality of life, physical function,

capacity to work, and ability to socialize

Appropriate monitoring and treatment of laboratory

abnormalities of CKD associated with implications for

health (e.g., anemia, CKD-MBD, potassium disorders, acidosis)

•

CKD outcomes

Minimize risk of progression to kidney failure

Manage risk and appropriate treatment of

complications, including cardiovascular diseases,

hospitalization, gout, infections, etc.

•

Modication of the natural course

of CKD and its symptoms

Figure 17 | Chronic kidney disease (CKD) treatment and risk modiﬁcation. CKD-MBD, chronic kidney disease-mineral and bone disorders.

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3.2.2 Physical activity and optimum weight

The Work Group concurs with all the recommendation and practice points relating to physical activity from the KDIGO 2022

Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease

and considers that they should extend to all

adults with CKD. We draw attention to the following statements:

Recommendation 3.2.2.1: We recommend that people with CKD be advised to undertake moderate-intensity

physical activity for a cumulative duration of at least 150 minutes per week, or to a

level compatible with their cardiovascular and physical tolerance (1D).

Practice Point 3.2.2.1: Recommendations for physical activity should consider age, ethnic background, presence of other

comorbidities, and access to resources.

Practice Point 3.2.2.2: People with CKD should be advised to avoid sedentary behavior.

Practice Point 3.2.2.3: For people at higher risk of falls, healthcare providers should provide advice on the intensity of physical

activity (low, moderate, or vigorous) and the type of exercises (aerobic vs. resistance, or both).

Practice Point 3.2.2.4: Physicians should consider advising/encouraging people with obesity and CKD to lose weight.

Special considerations

Pediatric considerations.

Practice Point 3.2.2.5: Encourage children with CKD to undertake physical activity aiming for World Health Organization

(WHO)-advised levels (i.e., ‡60 minutes daily) and to achieve a healthy weight.

3.3 Diet

Practice Point 3.3.1: Advise people with CKD to adopt healthy and diverse diets with a higher consumption of plant-based

foods compared to animal-based foods and a lower consumption of ultraprocessed foods.

Practice Point 3.3.2: Use renal dietitians or accredited nutrition providers to educate people with CKD about dietary

adaptations regarding sodium, phosphorus, potassium, and protein intake, tailored to their indi-

vidual needs, and severity of CKD and other comorbid conditions.

3.3.1 Protein intake

Recommendation 3.3.1.1: We suggest maintaining a protein intake of 0.8 g/kg body weight/d in adults with

CKD G3–G5 (2C).

Practice Point 3.3.1.1: Avoid high protein intake (>1.3 g/kg body weight/d) in adults with CKD at risk of progression.

Practice Point 3.3.1.2: In adults with CKD who are willing and able, and who are at risk of kidney failure, consider

prescribing, under close supervision, a very low–protein diet (0.3–0.4 g/kg body weight/d) sup-

plemented with essential amino acids or ketoacid analogs (up to 0.6 g/kg body weight/d).

Practice Point 3.3.1.3: Do not prescribe low- or very low–protein diets in metabolically unstable people with CKD.

Special considerations

Pediatric considerations.

Practice Point 3.3.1.4: Do not restrict protein intake in children with CKD due to the risk of growth impairment. The

target protein and energy intake in children with CKD G2–G5 should be at the upper end of the

normal ran ge for healthy children to promote optimal growth.

Older adults.

Practice Point 3.3.1.5: In older adults with underlying conditions such as frailty and sarcopenia, consider higher protein

and calorie dietary targets.

3.3.2 Sodium intake

The Work Group concurs with the following recommendation from KDIGO 2022 Clinical Practice Guideline for Diabetes

Management in Chronic Kidney Disease

and the KDIGO 2021 Clinical Practice Guideline for the Management of Blood

Pressure in Chronic Kidney Disease.

Recommendation 3.3.2.1: We suggest that sodium intake be <2 g of sodium per day (or <90 mmol of sodium

per day, or <5 g of sodium chloride per day) in people with CKD (2C).

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Practice Point 3.3.2.1: Dietary sodium restriction is usually not appropriate for patients with sodium-wasting nephropathy

Special considerations

Pediatric considerations.

Practice Point 3.3.2.2: Follow age-based Recommended Daily Intake when counseling about sodium intake for children with

CKD who have systolic and/or diastolic blood pressure >90th percentile for age, sex, and height.

3.4 Blood pressure control

The Work Group concurs with the KDIGO 2021 Clinical Practice Guideline fo r the Management of Blood Pressure in Chronic

Kidney Disease, which encourages individualized BP targets and the use of agents according to age, coexistent CVD, and other

comorbidities; risk of progression of CKD; and tolerance to treatments.

We highlight the following guidance:

Recommendation 3.4.1: We suggest that adults with high BP and CKD be treated with a target systolic blood pressure

(SBP) of <120 mm Hg, when tolerated, using standardized ofﬁce BP measurement (2B).

Practice Point 3.4.1: Consider less intensive BP-lowering therapy in people with frailty, high risk of falls and fractures,

very limited life expectancy, or symptomatic postural hypotension.

Special considerations

Pediatric considerations.

The Work Group concurs with the KDIGO 2021 Clinical Practice Guideline fo r the Management of Blood Pressure in Chronic

Kidney Disease, and we highlight the following guidance

Recommendation 3.4.2: We suggest that in children with CKD, 24-hour mean arterial pressure (MAP) by

ambulatory blood pressure monitoring (ABPM) should be lowered to £50th percentile

for age, sex, and height (2C).

Practi ce Po i nt 3. 4.2 : Monitor BP once a year with ABPM and every 3 – 6 m onths with standardized ausc ultatory of ﬁce

BP in children with CKD.

Practice Po int 3.4.3 : In children with CKD, when ABPM is not available, it is reasonable to target manual auscultatory

ofﬁce SBP, obtained in a protocol-driven standardized setting, of 50th–75th percentile for age, sex, and

height unless achieving this target is limited by signs or symptoms of hypotension.

3.5 Glycemic control

Please refer to the KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease for speciﬁc

recommendations, practice points, and research recommendations.

3.6 Renin-a ngiotensin system inhibitors

The Work Group highlights recommendations from the KDIGO 2021 Clinical Practice Guideline for the Management of Blood

Pressure in Chronic Kidney Disease and selected practice points for treatment with RASi from the KDIGO 2021 Clinical

Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease

and the KDIGO 2022 Clinical

Practice Guideline for Diabetes Management in Chronic Kidney Disease.

The Work Group considers several

recommendations to apply even in the absence of high BP and has adapted the recommendations from the BP guideline to

remove this requirement. Key recommendations and practice points are highlighted:

Recommendation 3.6.1: We recommend starting renin-angiotensin-system inhibitors (RASi) (an giotensin-con-

verting enzyme inhibitor [ACEi] or angiotensin II receptor blocker [ARB]) for people

with CKD and severely increased albumi nuria (G1–G4, A3) without diab etes (1B).

Recommendation 3.6.2: We suggest starting RASi (ACEi or ARB) for people with CKD and moderately increased

albuminuria (G1–G4, A2) without diabetes (2C).

Recommendation 3.6.3: We recommend starting RASi (ACEi or ARB) for people with CKD and moderately-to-

severely increased albuminuria (G1–G4, A2 and A3) with diabetes (1B).

Recommendation 3.6.4: We recommend avoiding any combination of ACEi, ARB, and direct renin inhibitor

(DRI) therapy in people with CKD, with or without diabete s (1B).

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Practice Point 3.6.1: RASi (ACEi or ARB) should be administered using the highest approved dose that is tolerated to

achieve the beneﬁts described because th e proven beneﬁts were achieved in trials using these doses.

Practice Point 3.6.2: Changes in BP, serum creatinine, and serum potassium should be checked within 2–4 weeks of

initiation or increase in the dose of a RASi, depending on the current GFR and serum potassium.

Practice Point 3.6.3: Hyperkalemia associated with use of RASi can often be managed by measures to reduce the serum

potassium levels rather than decreasing the dose or stopping RASi.

Practice Point 3.6.4: Continue ACEi or ARB therapy unless serum creatinine rises by more than 30% within 4 weeks

following initiation of treatment or an increase in dose.

Practice Point 3.6.5: Consider reducing the dose or discontinuing ACEi or ARB in the setting of either symptomatic hy-

potension or uncontrolled hyperkalemia despite medical treatment, or to reduce uremic symptoms

while treating kidney failure (estimated glomerular ﬁltration rate [eGFR] <15 ml/min per 1.73 m

Practice Point 3.6.6: Consider starting people with CKD with normal to mildly increased albuminuria (A1) on RASi (ACEi or

ARB) for speciﬁc indications (e.g., to treat hypertension or heart failure with low ejection fraction).

Practice Point 3.6 .7: Continue ACEi or ARB in people with CKD even when the eGFR falls below 30 ml/min per 1.73 m

3.7 Sodium-glucose cotransporter-2 inhibitors (SGLT2i)

The Work Group concurs w ith the KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney

Disease, which stated: “We recommend treating patients with type 2 diabetes (T2D), CKD, and an eGFR $20 ml/min per

1.73 m

with an SGLT2i (1A).”

However, in the present guideline, we offer a more general 1A recommendation for adults with

CKD. We also highlight practice points from the KDIGO Diabetes guideline for diabetes management in CKD, which are also

relevant for people with CKD without diabetes:

Recommendation 3.7.1: We recommend treating patients with type 2 diabetes (T2D), CKD, and an eGFR ‡20 ml/

min per 1.73 m

with an SGLT2i (1A).

Practice Point 3.7.1: Once an SGLT2i is initiated, it is reasonable to continue an SGLT2i even if the eGFR falls below

20 ml/min per 1.73 m

, unless it is not tolerated or KRT is initi ated.

Practice Point 3.7.2: It is reasonable to withhold SGLT2i during times of prolonged fasting, surgery, or critical medical

illness (when people may be at greater risk for ketosis).

Recommendation 3.7.2: We recommend treating adults with CKD with an SGLT2i for the following (1A):

 eGFR ‡20 ml/min per 1.73 m

with urine ACR ‡200 mg/g (‡20 mg/mmol), or

 heart failure, irrespectiv e of level of albuminuria.

Practice Point 3.7.3: SGLT2i initiation or use does not necessitate alteration of frequency of CKD monitoring and the

reversible decrease in eGFR on initiation is generally not an indication to discontinue therapy.

Recommendation 3.7.3: We suggest treating adults with eGFR 20 to 45 ml/min per 1.73 m

with urine ACR

<200 mg/g (<20 mg/mmol) with an SGLT2i (2B).

3.8 Mineralocorticoid receptor antagonists (MRA)

The Work Group highlights a key recommendation and practice points from the KDIGO 2022 Clinical Practice Guideline for

Diabetes Management in Chronic Kidney Disease.

Recommendation 3.8.1: We suggest a nonsteroidal mineralocorticoid receptor antagonist with proven kidney

or cardiovascular beneﬁt for adults with T2D, an eGFR >25 ml/min per 1.73 m

, normal

serum potassium concentration, and albuminuria (>30 mg/g [>3 mg/mmol]) despite

maximum tolerated dose of RAS inhibitor (RASi) (2A).

Practice Point 3.8.1: Nonsteroidal MRA are most appropriate for adults with T2D who are at high risk of CKD progression

and cardiovascular events, as demonstrated by persistent albuminuria despite other standard-of-care

therapies.

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Practice Point 3.8.2: A nonsteroidal MRA may be added to a RASi and an SGLT2i for treatment of T2D and CKD in adults.

Practice Point 3.8.3: To mitigate risk of hyperkalemia, select people with consistently normal serum potassium concen-

tration and monitor serum potassium regularly after initiation of a nonsteroidal MRA (Figure 26).

Practi ce Point 3.8.4: The choice of a nonsteroidal MRA should prioritize agents with documented kidney or

cardiovascular beneﬁts.

Practice Point 3.8.5: A steroidal MRA may be used for treatment of heart failure, hyperaldosteronis m, or refractory

hypertension, but may cause hyperkalemia or a reversible decline in glomerular ﬁlt ration, particularly

among people with a low GFR.

3.9 Glucagon-like peptide-1 receptor agonists (GLP-1 RA)

The Work Group highlights a key recommendation and practice point from the KDIGO 2022 Clinical Practice Guideline for

Diabetes Management in Chronic Kidney Disease.

Recommendation 3.9.1: In adults with T2D and CKD who have not achieved individualized glycemic targets

despite use of metformin and SGLT2 inhibitor treatment, or who are unable to use

those medications, we recommend a long-acting GLP-1 RA (1B).

Practice Point 3.9.1: The choice of GLP-1 RA should prioritize agents with documented cardiovascular beneﬁts.

3.10 Metabolic acidosis

Practice Point 3.10.1: In people with CKD, consider use of pha rmacological treatment with or without dietary

intervention to prevent develo pment of acidosis with potential clinical implications (e.g., serum

bicarbonate <18 mmol/l in adults).

Practice Point 3.10.2: Monitor treatment for metabolic acidosi s to ensure it does not result in serum bicarbonate

concentrations exceeding the upper limit of normal and does not adversely affect BP control,

serum potassium, or ﬂuid status.

3.11 Hyperkalemia in CKD

3.11.1 Awareness of factors impacting on potassium measurement

Practice Point 3.11.1.1: Be aware of the variability of potassium laboratory measurements as well as factors and mech-

anisms that may inﬂuence potassium measurement including diurnal and seasonal variation,

plasma versus serum samples, and the actions of medications.

3.11.2 Potassium exchange agents

Practice Point 3.11.2.1: Be aware of local availability or formulary restrictions with regard to the pharmacologic man-

agement of nonemergent hyperkalemia.

3.11.3 Timing to recheck potassium after identifying moderate and severe hyperkalemia in adults

[No recommendations and practice points]

≤4.8 mmol/l K

4.9–5.5 mmol/l

>5.5 mmol/l

• Initiate nerenone

- 10 mg daily if eGFR 25–59 ml/min/1.73 m

- 20 mg daily if eGFR ≥60 ml/min/1.73 m

• Monitor K

at 1 month after initiation and then every 4

months

• Increase dose to 20 mg daily, if on 10 mg daily

• Restart 10 mg daily if previously held for hyperkalemia and

now ≤5.0 mmol/l

• Continue nerenone 10 mg or 20 mg

• Monitor K

every 4 months

• Hold nerenone

• Consider adjustments to diet or concomitant

medications to mitigate hyperkalemia

• Recheck K

• Consider reinitiation if/when K

≤5.0 mmol/l

Figure 26 | Serum potassium monitoring during treatment with a nonsteroidal mineralocorticoid receptor antagonist (MRA)

(ﬁnerenone). Adapted from the protocols of Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease (FIDELIO-

DKD) and Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD). The Work Group considers

these potassium thresholds to be conservative, and it may be considered appropriate to continue MRAs in people with potassium of 5.5–6.0 mmol/

l. This algorithm could be used for steroidal MRA. The US Food and Drug Administration (FDA) has approved initiation of K

< 5.0 mmol/l. This

ﬁgure is guided by trial design and the FDA label and may be different in other countries. Serum creatinine/estimated glomerular ﬁltration rate

(eGFR) should be monitored concurrently with serum potassium. Reproduced from Kidney Disease: Improving Global Outcomes Diabetes Work

Group. KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. Kidney Int. 2022;102:S1–S127.

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3.11.4 Managing hyperkalemia

[No recommendations and practice points]

3.11.5 Dietary considerations

Practice Point 3.11.5.1: Implement an individualized approach in people with CKD G3–G5 and emergent hyperkalemia that

includes dietary and pharmacologic interventions and takes into consideration associated comor-

bidities and quality of life (QoL). Assessment and education through a renal dietitian or an accredited

nutrition provider are advised.

Practice Point 3.11.5.2: Provide advice to limit the intake of foods rich in bioavailable po tassium (e.g., processed foods)

for people with CKD G3–G5 who have a history of hyperkalemia or as a prevention strategy

during disease periods in which hyperkalemia risk may be a concern.

3.12 Anemia

The KDIGO 2012 Clinical Practice Guideline for Anemia in Chronic Kidney Disease will be updated in 2024.

437

3.13 CKD-Mineral Bone Disorder (CKD-MBD)

The Work Group highlig hts the KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and

Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).

Please refer to this publication for speciﬁc

recommendations, selection, dosing of speciﬁc therapeutic agents, and research recommendations.

3.14 Hyperuricemia

Recommendation 3.14.1: We recommend people with CKD and symptomatic hyperuricemia should be offered

uric acid–lowering intervention (1C).

Practi ce Point 3.14.1: Consider initiating uric acid–lowering therapy for people with CKD after their ﬁrst episode of gout

(particularly where there is no avoidable precipitant or serum uric acid concentration is >9 mg/dl

[535

mol/l]).

Practice Point 3.14.2 : Prescribe xanthine oxidase inhibitors in preference to uricosuric agents in people with CKD and

symptomatic hyperuricemia.

Practice Point 3.14.3: For symptomatic treatment of acute gout in CKD, low-dose colchicine or intra-articular/oral glu-

cocorticoids are preferable to nonsteroidal anti-inﬂammatory drugs (NSAIDs).

Dietary approaches.

Practice Point 3.14.4: Nonpharmacological interventions which may help prevent gout include limiting alcohol, meats, and

high-fructose corn syrup intake.

Recommendation 3.14.2: We suggest not using agents to lower serum uric acid in people with CKD and

asymptomatic hyperuricemia to delay CKD progression (2D).

3.15 Cardiovascular disease (CVD) and additional speciﬁc interventions to modify risk

3.15.1 Lip id management

The beneﬁts of lowering LDL cholesterol using statin-based therapies on the risk of ASCVD are well established in people with

and without CKD. There are clear recommendations on when to initiate such therapies set out in the KDIGO Clinical Practice

Guideline for Lipid Management in Chronic Kidney Disease.

The Work Group concurs with all the recommendations in this

guideline. In particular, we draw attention to:

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Recommendation 3.15.1.1: In adults aged ‡50 years with eGFR <60 ml/min per 1.73 m

but not treated with

chronic dialysis or kidney transplantation (GFR categories G3a–G5), we recom-

mend treatment with a statin or statin/ezetimibe combination (1A).

Recommendation 3.15.1.2: In adults aged ‡50 years with CKD and eGFR ‡60 ml/min per 1.73 m

(GFR cate-

gories G1– G2), we recommend treatment with a statin (1B).

Recommendation 3.15.1.3: In adults aged 18–49 years with CKD but not treated with chronic dialysis or kidney

transplantation, we suggest statin treatment in people with one or more of the

following (2A):

 known coronary disease (myocardial infarction or coronary revascularization),

 diabetes mellitus,

 prior ischemic stroke, or

 estimated 10-year incidence of coronary death or nonfatal myocardial infarction

>10%.

Practice Point 3.15.1.1: Estimate 10-year cardiovascular risk using a validated risk tool.

Practice Point 3.15.1.2: In people with CKD, choose statin-based regimens to maximize the absolute reduction in low-

density lipoprotein (LDL) cholesterol to achieve the largest treatment beneﬁts.

Practice Point 3.15.1.3: In adults with CKD aged 18–49, a lower (i.e., <10%) estimated 10-year incidence of coronary death

or nonfatal myocardial infarction may also be appropriate thresholds for initiation of statin-based

therapy.

Practice Point 3.15.1.4: Consider prescribing proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors to people

with CKD who have an indication for their use.

Dietary approaches.

Practice Point 3.15.1.5: Consider a plant-based “Mediterranean-style” diet in addition to lipid-modifying therapy to reduce

cardiovascular risk.

3.15.2 Use of antiplatelet therapy

Recommendation 3.15.2.1: We recommend oral low-dose aspirin for prevention of recurrent ischemic cardio-

vascular disease events (i.e., secondary prevention) in people with CKD and

established ischemic cardiovascular disease (1C).

Practice Point 3.15.2.1: Consider other antiplatelet therapy (e.g., P2Y

inhibitors) when there is aspirin intolerance.

3.15.3 Invasive versus intensive medical therapy for coronary artery disease

Recommendation 3.15.3.1: We suggest that in stable stress-test conﬁrmed ischemic heart disease, an initial

conservative approach using intensive medical therapy is an appropriate alterna-

tive to an initial invasive strategy (2D).

Practice Point 3.15.3.1: Initial management with an invasive strategy may still be preferable for people with CKD with

acute or unstable coronary disease, unacceptable levels of angina (e.g., patient dissatisfaction), left

ventricular systolic dysfunction attributable to ischemia, or left main disease.

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3.16 CKD and atrial ﬁbrillation

Practice Point 3.16.1: Follow established strategies for the diagnosis and management of atrial ﬁbrillation (Figure 40).

Recommendation 3.16.1: We recommend use of non–vitamin K antagonist oral anticoagulants (NOACs) in

preference to vitamin K antagonists (e.g., warfarin) for thromboprophylaxis in atrial

ﬁbrillation in people with CKD G1–G4 (1C).

Practice Point 3.16.2: NOA C dose adjustment for GFR is required, with caution needed at CKD G4–G5.

Practice Point 3.16.3: Duration of NOAC discontinuation before elective procedures needs to consider procedural bleeding

risk, NOAC prescribed, and level of GFR (Figure 44).

Step 1

Diagnosis

• In people with CKD, use opportunistic pulse-based screening (e.g., taking at when measuring BP), followed by a

wearable device or Holter ECG testing

Step 2

Prophylaxis against

stroke and systemic

thromboembolism

(they are likely to have an increased CHA

-VASc risk factor for stroke and are at high risk even with a score of 0–1)

managed (e.g., alcohol advice, use of a proton pump inhibitor)

Step 3

Rate/rhythm control

†

• Use medical therapy (e.g., beta blockade) to control ventricular rate to less than about 90 bpm at rest to decrease

symptoms and related complications

• For people with persistent symptoms despite adequate rate control, consider rhythm control with cardioversion,

antiarrhythmic therapy and/or catheter ablation

Figure 40 | Strategies for the diagnosis and management of atrial ﬁbrillation. *Consider dose adjustments necessary in people with

chronic kidney disease (CKD).

†

The following has been recommended as a standard package for diagnostic evaluation of new atrial ﬁbrillation:

(i) a 12-lead electrocardiogram (ECG) to establish the diagnosis, assess ventricular rate, and check for the presence of conduction defects,

ischemia, or structural heart disease; (ii) laboratory testing for thyroid and kidney function, serum electrolytes, and full blood count; and (iii)

transthoracic echocardiography to assess left ventricular size and function, left atrial size, for valvular disease, and right heart size and function.

BP, blood pressure; CHA

-VASc, Congestive heart failure, Hypertension, Age $75 (doubled), Diabetes, Stroke (doubled), Vascular disease,

Age 65 to 74, and Sex category (female); HAS-BLED, Hypertension, Abnormal liver/kidney function, Stroke history, Bleeding history or

predisposition, Labile international normalized ratio (INR), Elderly, Drug/alcohol usage.

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Chapter 4: Medication management and drug stewardship in CKD

4.1 Medication choices and monitoring for safety

Practice Point 4.1.1: People with CKD may be more susceptible to the nephrotoxic effects of medications. When prescribing

such medications to people with CKD, always consider the beneﬁts versus potential harms.

Practice Point 4.1.2: Monitor eGFR, electrolytes, and therapeutic medication levels, when indicated, in people with CKD

receiving medications with narrow therapeutic win dows, potential adverse effects, or nephrotoxicity,

both in outpatient practice and in hospital settings.

Practice Point 4.1.3: Review and limit the use of over-the-co unter medicines and dietary or herbal remedies that may be

harmful for people with CKD.

Medications and pregnancy.

Practice Point 4.1.4: When prescribing medications to people with CKD who are of child-bearing potential, always review

teratogenicity potential and provide regular reproductive and contraceptive counseling in accordance

with the values and preferences of the person with CKD.

4.2 Dose adjustments by level of GFR

Practice Point 4.2.1: Consider GFR when dosing medications cleared by the kidneys.

Practice Point 4.2.2: For most people and clinical settings, validated eGFR equations using SCr are appropriate for drug

dosing.

Practice Point 4.2.3: Where more accuracy is required for drug-related decision-making (e.g., dosing due to narrow ther-

apeutic or toxic range), drug toxicity, or clinical situations where eGFRcr estimates may be unreliable,

use of equations that combine both creatinine and cystatin C, or measured GFR may be indicated.

Apixaban–Edoxaban–RivaroxabanDabigatran

Low risk High risk

No important bleeding risk and/or adequate local hemostasis possible:

perform at trough level (i.e., ≥12 or 24 h after last intake)

Low risk High risk

CrCl ≥80 ml/min ≥24 h ≥48 h ≥24 h ≥48 h

CrCl 50–80 ml/min ≥36 h ≥72 h ≥24 h ≥48 h

CrCl 30–50 ml/min

≥48 h ≥96 h ≥24 h ≥48 h

CrCl 15–30 ml/min

No ocial indication No ocial indication ≥36 h ≥48 h

CrCl <15 ml/min No ocial indication for use

There is no need for bridging with LMWH/UFH

Figure 44 | Advice on when to discontinue non–vitamin K antagonist oral anticoagulants (NOACs) before procedures (low vs. high risk).

The bold values deviate from the common stopping rule of $24-hour low risk, $48-hour high risk. Low risk is deﬁned as a low frequency of

bleeding and/or minor impact of a bleed. High risk is deﬁned as a high frequency of bleeding and/or important clinical impact. Adapted from

Heidbuchel H, Verhamme P, Alings M, et al. Updated European Heart Rhythm Association practical guide on the use of non–vitamin-K

antagonist anticoagulants in patients with non-valvular atrial ﬁbrillation: executive summary. Eur Heart J. 2017;38:2137–2149.

724 a

Many of these

people may be on lower dose of dabigatran (110 mg twice per day [b.i.d.]) or apixaban (2.5 mg b.i.d.), or have to be on the lower dose of

rivaroxaban (15 mg QD) or edoxaban (30 mg QD). Dabigatran 110 mg b.i.d. has not been approved for use by the US Food and Drug

Administration. CrCl, creatinine clearance, LMWH, low-molecular-weight heparin; UFH, unfractionated heparin. Reproduced from Turakhia MP,

Blankestijn PJ, Carrero JJ, et al. Chronic kidney disease and arrhythmias: conclusions from a Kidney Disease: Improving Global Outcomes

(KDIGO) Controversies Conference. Eur Heart J. 2018;39:2314–2325.

710

ª The Author(s) 2018. Published by Oxford University Press on behalf of

the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-

Commercial License (http://creativecommons.org/licenses/by-nc/4.0/).

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Practice Point 4.2.4: In people with extremes of body weight, eGFR nonindexed for body surface area (BSA) may be

indicated, especially for medications with a narrow therapeutic range or requiring a minimum

concentration to be effective.

Practice Point 4.2.5: Consider and adapt drug dosing in people where GFR, non-GFR determinants of the ﬁltration

markers, or volume of distribution are not in a steady state.

4.3 Polypharmacy and drug stewardship

Practice Point 4.3.1: Perform thorough medication review periodically and at transitions of care to assess adherence,

continued indication, and potential drug interactions because people with CKD often have complex

medication regimens and are seen by multiple specialists.

Practice Point 4.3.2: If medications are discontinued during an acute illness, communicate a clear plan of when to restart

the discontinued medications to the affected person and healthcare providers, and ensure docu-

mentation in the medical record.

Practi ce Poi nt 4.3.3: Consider planned discontinuation of medications (such as metformin, ACEi, ARBs, and SGLT2i) in

the 48–72 hours prior to elective surgery or during the acute management of adverse effects as a

precautionary measure to prevent complications. However, note that failure to restart these medi-

cations after the event or procedure may lead to unintentional harm (see Practice Point 4.3.2).

4.3.1 Strategies to promote drug stewardship

Practi ce Poin t 4.3.1.1: Educate and inform people with CKD regarding the expected beneﬁts and possible risks of medi-

cations so that they can identify and report adverse events that can be managed.

Practice Point 4.3.1.2: Establish collaborative relationships with other healthcar e providers and pharmacists and/or

use tools to ensure and improve drug stewardship in people with CKD to enhance manageme nt

of their complex medicati on reg imens.

4.4 Imaging studies

Practice Point 4.4.1: Consider the indication for imaging studies in accordance with general population in-

dications. Risks and beneﬁts of imaging stud ies should be determined on an ind ividual

basis in the context of their CKD.

4.4.1 Radi ocontrast: intra-arterial and intravenous dye studies

Practice Point 4.4.1.1: Assess the risk for AKI in people with CKD receiving intra-arterial contrast for cardiac pro-

cedures using validated tools.

Practice Point 4.4.1.2: The intravenous administration of radiocontrast media can be managed in accordance with

consensus statements from the radiol ogy societies in people with AKI or GFR <60 ml/min per 1.73

(CKD G3a–G5) undergoing elective investigation.

4.4.2 Gadolinium-containing contrast media

Practice Point 4.4.2.1: For people with GFR <30 ml/min per 1.73 m

(CKD G4–G5) who require gadolinium-containing

contrast media, preferentially offer them A merican College of Radiology group II and III

gadolinium-based contrast agents.

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Chapter 5: Optimal models of care

5.1 Referral to specialist kidney care services

Practice Point 5.1.1: Refer adults with CKD to specialist kidney care services in the circu mstances listed in Figure 48.

Special considerations

Pediatric considerations.

Practice Point 5.1.2: Refer children and adolescents to specialist kidney care services in the following circumstances:

 an ACR of 30 mg/g (3 mg/mmol) or a PCR of 200 mg/g (20 mg/mmol) or more, conﬁrmed on a

repeat ﬁrst morning void sample, when well and not during menstruation,

 persistent hematuria,

 any sustained decrease in eGFR,

 hypertension,

 kidney outﬂow obstruction or anomalies of the kidney and urinary tract,

 known or suspected CKD, or

 recurrent urinary tract infection.

5.2 Symptoms in CKD

5.2.1 Prevalence and severity of symptoms

[No recommendations and practice points]

5.2.2 Identiﬁcation and assessment of symptoms

Practice Point 5.2.2.1: Ask people with progressive CKD about uremic symp toms (e.g ., reduced appetite, nausea, and level

of fatigue/lethargy) at each consultation using a standardized validated assessment of uremic

symptoms tool.

Further evaluation and

specialist management

based on diagnosis

Causes

Circumstances category Circumstance examples Actions

Diagnosis of CKD

eGFR/risk of KRT

Planning and preparation

for kidney replacement

therapy

Albuminuria

and microscopic

hematuria

Further evaluation

and management

Others

Management of CKD

complications

• Cause of CKD is uncertain

• Hereditary kidney disease

• Recurrent extensive nephrolithiasis

• A >3%–5% 5-year risk of requiring KRT measured

using a validated risk equation

• eGFR <30 ml/min per 1.73 m

• A sustained fall in GFR of >20% or >30% in those

people initiating hemodynamically active therapies

• Consistent nding of signicant albuminuria

(ACR ≥300 mg/g [≥30 mg/mmol] or AER ≥300 mg/24 hours,

approximately equivalent to PCR ≥500 mg/g [≥50 mg/mmol]

or PER ≥500 mg/24 h) in combination with hematuria

• ≥2-fold increase in albuminuria in people with signicant

albuminuria undergoing monitoring

• A consistent nding of ACR >700 mg/g [>70 mg/mmol]

• Urinary red cell casts, RBC >20 per high power eld

sustained and not readily explained

• CKD and hypertension refractory to treatment

≥4 antihypertensive agents

• Persistent abnormalities of serum potassium

• Acidosis

• Anemia

• Bone disease

• Malnutrition

Figure 48 | Circumstances for referral to specialist kidney care services and goals of the referral. ACR, albumin-to-creatinine ratio; AER,

albumin excretion rate; CKD, chronic kidney disease; eGFR, estimated glomerular ﬁltration rate; KRT, kidney replacement therapy; PCR, protein-

creatinine ratio; PER, protein excretion rate; RBC, red blood cells.

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5.2.3 Management of common symptoms for people with CKD

Practice Point 5.2. 3.1: Use evidence-informed management strategies to support people to live well with CKD and improve

their health-related quality of life.

Practice Point 5.2.3.2: Screen people with CKD G4–G5, aged >65, poor growth (pediatrics), or symptoms such as

involuntary weight loss, frailty, or poor appetite twice annually for malnutrition using a

validated assessm ent to ol.

Practi ce Poin t 5.2.3.3: Enable availability of appropriate medical nutrition therapy for people with signs of malnutrition,

ideally under the supervision of renal dietitians or accredited nutrition providers if not available.

5.3 Team-b ased integrated care

Practice Point 5.3.1: Enable access to a patient-centered multidisciplinary care team consisting of dietary counseling,

medication management, education, and counseling about different KRT modalities, transplant

options, dialysis access surgery, and ethical, psychological, and social care for people with CKD.

Practice Point 5.3.2: Education programs that also involve care partners where indicated are important to promote

informed, activated people with CKD.

Practice Point 5.3.3: Consider the use of telehealth techno logies including web-based, mobile applications, virtual

visiting, and wearable devices in the delivery of education and care.

Special considerations

Pediatric considerations.

5.3.1 Transition from pediatric to adult care

5.3.1.1 Pediatric providers

Practice Point 5.3.1.1.1: Prepare adolescents and their families for transfer to adult-oriented care starting at 11–14 years of age

by using checklists to assess readiness and guide preparation, and by conducting part of each visit

without the parent/guardian present (Figure 55).

Practice Point 5.3.1.1.2: Provide a comprehensive written transfer summary, and ideally an oral handover, to the receiving

healthcare providers including all relevant medical information as well as informa tion about the

young person’s cognitive abilities and social support (Figure 55).

Practice Point 5.3.1.1.3: Transfer young people to adult care during t imes of medical and social stability where poss ible.

5.3.1.2 Adult providers

Practice Point 5.3.1.2.1: Recognize that young people under 25 years of age with CKD are a unique population at high risk for

adverse outcomes at least in part due to physiologic incomplete brain maturation.

Practice Point 5.3.1.2.2: Encourage young people to informally visit the adult care clinic to which they will be transferred

before the ﬁrst appointment (Figure 55).

Transition

Preparation for transfer

Pediatric care

Preparation for regular adult care

Joint pediatric-adult care

Young adult care

Transition

Regular

adult care

Transfer – when stable

• Allow young people to visit the clinic before transfer

• Recognize that “emerging adulthood” is a period of

high risk for adverse outcomes

• See emerging adults more frequently than older adults

with same stage of CKD

• Include caregivers or signicant others in patient visits,

with permission of patient

Age (years)

11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26

• Start early (11–14 yr)

• Use checklists to assess readiness

and guide preparation

• See young person alone for

at least part of each visit

• Comprehensive written

summary and verbal

handover, including

cognitive ability and

social support

• Follow-up after transfer

Figure 55 | The process of transition from pediatric to adult care in chronic kidney disease (CKD).

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Practice Point 5.3.1.2.3: Assess young people with CKD more frequently than older people with the same stage of CKD and,

with the agreement of the young person, include the caregivers or signiﬁcant other of the young

person in their care, at least in the ﬁrst 1–3 years following transfer from pediatric care (Figure 55).

5.4 Timing the initiation of dialysis

Practice Point 5.4.1: Initiate dialysis based on a composite assessment of a person’s symptoms, signs, QoL, preferences,

level of GFR, and laboratory abnormalities.

Practice Point 5.4.2: Initiate dialysis if the presence of one or more of the following situations is e vident ( Table 41).

This often but not invariably occurs in the GFR ran ge between 5 and 10 ml/mi n per 1.73 m

Practice Point 5.4.3: Consider planning for preemptive kidney transplantation and/or dialysis access in adults when the

GFR is <15–20 ml/min per 1.73 m

or risk of KRT is >40% over 2 years.

Special considerations

Pediatric considerations.

Practice Point 5.4.4: In children, in addition to the adult indications for dialysis, poor growth refractory to optimized

nutrition, growth hormone, and medical management is an indication for initiating KRT.

Practice Point 5.4.5: Pursue living or deceased donor preemptive kidney transplantation as the treatment of choice for

children in whom there is evidence of progressive and irreversible CKD. The eGFR at which pre-

emptive transplantation should be undertaken will depend on multiple factors including the age and

size of the child and the rate of progression of kidney failure but will usually be between 5–15 ml/min

per 1.73 m

5.5 Structure and process of supportive care and comprehensive conservative management

Practice Point 5.5.1: Inform people with CKD about the options for KRT and comprehensive conservative care.

Practice Point 5.5.2: Support comprehensive conservative management as an option for people who choose not to pursue

KRT.

Practice Point 5.5.3: Provide access to resources that enable the delivery of advanced care planning for people with a

recognized need for end-of-life care, including those people undergoing comprehensive conservative

care.

Table 41 | Indications for the initiation of dialysis

Symptoms or signs attributable to kidney failure (e.g., neurological signs and symptoms attributable to uremia, pericarditis, anorexia, medically resistant

acid-based or electrolyte abnormalities, intractable pruritus, serositis, and acid-base or electrolyte abnormalities)

Inability to control volume status or blood pressure

Progressive deterioration in nutritional status refractory to dietary intervention, or cognitive impairment

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Chapter 1: Evaluation of CKD

1.1 Detection and evaluation of CKD

Both decreased GFR and increased albuminuria or other

markers of kidney damage are often silent and not appare nt to

thepersonatriskofCKDorthehealthcareproviderunless

laboratory tests are performed. The cause of the decreased GFR

or increased albuminuria may also not be apparent. In the

decade since the publication of the previous KDIGO Clinical

Practice Guideline for the Evaluation and Management of

Chronic Kidney Disease,

there have been substantial advances

in treatment for CKD of all causes (Chapter 3), targeted

therapies for speciﬁc causes of CKD (e.g., KDIGO 2021

Clinical Practic e Guideline for the Management of

Glomerular Diseases

), as well as understanding of and

methods to determine the etiology of CKD. All together , these

advances have the potential to slow and possibly prev ent the

progression of kidney disease. Thus, in this section of Chapter

1, we emphasize the importance of detecting CKD, and

considerations for the optimal methods for staging of CKD,

and how to establish chronicity and etiology.

1.1.1 Detection of CKD

Practice Point 1.1.1.1: Test people at risk for and with chronic

kidney disease (CKD) using both urine albumin measurement

and assessment of glomerular ﬁltration rate (GFR).

Early detection of any chronic disease, including CKD,

provides greater opportunities to reduce morbidity as treat-

ments can be initiated earlier in the disease course. Because

treatments for CKD provide beneﬁts in reducing risk for both

CVD and CKD progression, strategies that promote early

detection of CKD should improve kidney and non–kidney-

related outcomes. Even if medical treatments are not available

or indicated for an individual, there are recommended lifestyle

changes that could be implemented after the diagnosis of CKD

(Chapter 3). Interviews with people who have CKD have pro-

vided evidence that many would alter their lifestyle if they

received a diagnosis of CKD.

Knowledge of level of

albuminuria and GFR also helps guide clinical decisions

beyond initiating treatments speciﬁcally for CKD (Table 4).

Each of these is considered in greater depth in the subsequent

chapters. Finally, if a familial form of kidney disease is

suspected, the diagnosis of the disease in one person may

allow detection in other family members. Thus, in itial testing

of blood and urine to detect CKD is important, with

conﬁrmatory testing if initial ﬁndings indicate the presence of

abnormalities of creatinine/eGFR or albuminuria.

From a societal perspective, early identiﬁcation of and

intervention for CKD could have a positive impact on health

disparities. In many countries, there is a higher incidence of CKD

among people with lower SES, and these people are more likely

to progress to kidney failure and have less access to KRT (dialysis

Table 4 | Use of GFR and albuminuria

Clinical decisions

Current level

Change in the level of GFRGFR Albuminuria

Diagnosis and

staging

 Detection of CKD

 Evaluation for kidney donation

 Detection of CKD  Detection of AKI and AKD

 Detection of CKD progression

Treatment

 Referral to nephrologists

 Patient and family education about CKD

and beneﬁt of lifestyle changes

 Monitor progression of GFR decline

 Referral for kidney transplantation

 Placement of dialysis access

 Dosage and monitoring for medications

cleared by the kidney

 Determine safety of diagnostic tests or procedures

 Eligibility for clinical trials

 Referral to nephrologists

 Patient and family education about

CKD and beneﬁt of lifestyle changes

 Monitor progression of GFR decline

 Eligibility for clinical trials

 Treatment of AKI

 Monitoring drug toxicity

 Re-evaluate CKD treatment

strategies

Risk assessment

 Risk of CKD complications

 Risk for CKD progression

 Risk of CVD

 Risk for medication errors

 Risk for perioperative complications

 Risk for mortality

 Fertility and risk of complications

of pregnancy

 Risk for CKD progression

 Risk for CVD

 Risk for mortality

 Fertility and risk of complications

of pregnancy

 Risk for kidney failure

 Risk for CVD, HF, and mortality

 Risk for adverse pregnancy

outcome

AKD, acute kidney disease; AKI, acute kidney injury; CKD, chronic kidney disease; CVD, cardiovascular disease; GFR, glomerular ﬁltration rate; HF, heart failure.

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and transplantation).

A public health approach toward CKD

detection and treatment could reduce inequities in the burden

of kidney failure by slowing the rate of progression and the

risk of CVD for everyone.

The possible harm of early detection of CKD is that the

new diagnosis may cause anxiety in some people, particularly

if the testing is not discussed in advance of the results. Dis-

cussions around disease detection are common in the primary

care setting, and shared decision-making is an established

practice through which people may agree to the testing,

conﬁrm that they would like to be tested, and prepare for the

range of possible results and their implications.

58–60

Early

detection increases burden and costs associated with physi-

cian visits or treatments, and this may not be balanced by

savings from averting adverse outcomes.

CKD ﬁts the World Health Organization (WHO) criteria for

an early detection program.

61–63

Given that chronic disease

detection and prevention frameworks have been deployed for

other disease and risk factor conditions, in our view, CKD

detection strategies should be implemented for high-risk people.

A framework has been developed for communities to align

CKD detection and treatment strategies within their broader

public health priorities to ensure that the goals of the interven-

tion are achieved without compromising other valuable health

initiatives.

Both the efﬁcacy and the cost-effectiveness of CKD

detection and treatment interventions will depend upon the

speciﬁc strategies that are employed in the healthcare system.

Therefore, results from future clinical trials should be

evaluated within their unique context and may not generalize

to all CKD detection efforts.

Most people with or at risk for CKD, healthcare providers, and

policy makers would wish to identify CKD. Most people who are

already receiving medical care would choose case-ﬁnding stra-

tegies to enable earlier risk stratiﬁcation and treatment for pre-

viously undiagnosed CKD.

17,64

Thus, the application of earlier

treatment to delay CKD progression in people with CKD is of

a higher priority than the lack of clinical trial evidence that

case-ﬁnding strategies themselves improve outcomes.

This practice point promoting CKD detection efforts may

have implications for health equity, because CKD dispro-

portionately affects people from minoritized populations and

those who have lower SES. The increasing availability and

evidence supporting several treatments for CKD advocates for

early disease detection. Given the asymptomatic progression

of CKD, systematic testing of people with risk factors for

CKD is the only method that would detect CKD at early

stages and allow the initiation of appropriate treatments.

CKD detection could reduce the proportion of people with

CKD who will experience the morbidity of CKD G4–G5.

Cost-effectiveness analyses, performed in the new era of

effective disease-modifying therapies, describe a more positive

view of population-wide screening.

Figure 3

provides an algorithm for the identiﬁcation of

people at risk for CKD testing in those at risk, further

testing in those identiﬁed as havi ng CKD to conﬁrm stages,

and subsequently allowing for treatment initiation. Primary

care physicians or other medical specialists who care for

people with risk factors for CKD, such as endocrinology,

cardiology, or rheumatology, are ideal settings for an

intervention that targets people with undetected CKD.

Implementing an early detection intervention would be

facilitated by integrated healthcare systems and the use of

electronic health records. These structures would facilitate

the linkage between risk stratiﬁcation and treatment to have

the desired effect of slowing the progression of CKD.

The highest priority conditions for CKD detection are

hypertension, diabetes, and CVD, including heart failure. For

diabetes, the ADA and KDIGO recommend annual screening

of people with diabetes for CKD.

CKD screening should

start at diagnosis of T2D because evidence of CKD is often

already apparent at this time. For T1D, screening is

recommended commencing 5 years after diagnosis. A

second important group includes people with recent AKI or

acute kidney disease (AKD), particularly multiple episodes

of AKI, and those who have been “partially diagnosed” with

CKD by either eGFR or albuminuria but cannot be fully

staged. Other groups who might be considered for CKD

testing are shown in Table 5. This list is not exhaustive and

may be modiﬁed by local epidemiological considerations. As

per above, 2023 analyses suggest that population screening

may in fact be cost-effective, obviating the need for

“selecting” and addressing an ever-changing list of “at risk”

groups.

Testing for CKD without regard to age generates contro-

versy. Those in older age groups experience the greatest

burden of CKD and are also at the highest risk for cardio-

vascular complications. As with other detection programs like

cancer detection, CKD detection efforts should be individu-

alized based on the person’s goals of care and suitability for

treatment.

Practice Point 1.1.1.2: Following incidental detection of

elevated urinary albumin-to-creatinine ratio (ACR), he-

maturia, or low estimated GFR (eGFR), repeat tests to

conﬁrm pre sence of CKD.

There is known biological and analytical variability in SCr

and in urine albumin or urine protein not related to their

properties as markers of kidney disease. In people without

risk factors for CKD, there is a low pretest probability for

CKD. Thus, any unexpected results should be veriﬁed before

diagnosing a person as having CKD. In people with risk

factors for CKD, there is a higher probability that the person

does have CKD even with an unexpected ﬁnding. Subsequent

testing should be performed to conﬁrm the diagnosis and to

complete the evaluation, as is required. Timing of the repeat

sample should be determined based on clinical setting

including risk factors for CKD as well as concern for AKI/

AKD.

Hematuria is common and associated with risk for sub-

sequent development of CKD.

There are several causes of

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transient hematuria. Persistent hematuria may indicate

glomerular disease, other kidney diseases, or urologic

disease including genitourinary malig nancy. Thus, persistent

hematuria should prompt further investigation.

66,67

Special considerations

Pediatric considerations.

People who are born preterm,

especially if also small for gestational age, are at increased risk

for CKD and kidney failure. This is largely related to

decreased nephron number.

68–70

Additional insults after birth

such as neonatal AKI and childhood obesity can further in-

crease the risk of CKD.

71,72

1.1.2 Methods for staging of CKD

Recommendation 1.1.2.1: In adults at risk for CKD,

we recom mend using creatinine-based estimated

glomerular ﬁltration rate (eGFRcr). If cystatin C is

available, the GFR category should be estimated

from the combination of creatinine and cystatin C

(creatinine and cystatin C–based estimated glomer-

ular ﬁltration rate [eGFRcr-cys]) (1B) .

For the diagnosis and staging of CKD by GFR, this recom-

mendation puts a high value on data suggesting that the most

accurate method of estimating GFR is by using 2 biomarkers

(cystatin C and creatinine), as each has limitations and beneﬁts

as ﬁltration markers. As compared with mGFR, estimating

equations using both creatinine and cystatin C afford greater

accuracy in compa rison with either ﬁltration marker alone. The

recommendation places a lower value on the resource utilization

and cost associated with the assessment of eGFRcr-cys.

Key information

Balance of beneﬁts and harms.

In the CKD-PC collabora-

tion, 720,736 people had measures of blood cystatin C in addi-

tion to having eGFRcr and ACR.

Replacing the assessment of

eGFRcr with eGFRcr-cys in the matrix of GFR categories led

to several changes in the risk distributions. Most notably, the

group with an eGFR category 45–59 ml/min per 1.73 m

and

ACR <10 mg/g (<1 mg/mmol) was moved to higher risk for

all 10 outcomes, and this category was no longer labeled

as being low-risk (“green”) for any of the complications

(Figure 6

). For the 8 outcomes that are not inﬂuenced by

changes in creatinine (i.e. all except kidney failure and AKI),

eGFRcr exhibited a J-shaped association such that risk

increased with eGFR values >105 ml/min per 1.73 m

(Figure 7

). In contrast eGFRcr-cys demonstrated much

more linear associations with each of these complications

throughout its distribution. These data demonstrate that the

combined eGFRcr-cys equation is superior for distinguishing

GFR risk stages compared with eGFRcr.

Certainty of evidence. This recommendation is based on 2

broadly different types of data—data comparing the accuracy

) of equations from a combination of creatinine and

cystatin C as ﬁltration markers and creatinine and cystatin C

Table 5 | Risk factors for CKD

Domains Example conditions

Common risk factors Hypertension

Diabetes

Cardiovascular disease (including heart failure)

Prior AKI/AKD

People who live in geographical areas with

high prevalence of CKD

Areas with endemic CKDu

Areas with the high prevalence of APOL1 genetic variants

Environmental exposures

Genitourinary disorders Structural urinary tract disease

Recurrent kidney calculi

Multisystem diseases/chronic inﬂammatory

conditions

Systemic lupus erythematosus

Vasculitis

HIV

Iatrogenic (related to drug treatments and procedures) Drug-induced nephrotoxicity and radiation nephritis

Family history or known genetic variant

associated with CKD

Kidney failure, regardless of identiﬁed cause

Kidney disease recognized to be associated with genetic abnormality (e.g., PKD,

APOL1-mediated kidney disease, and Alport syndrome)

Gestational conditions Preterm birth

Small gestational size

Pre-eclampsia/eclampsia

Occupational exposures that promote CKD risk Cadmium, lead, and mercury exposure

Polycyclic hydrocarbons

Pesticides

AKD, acute kidney disease; AKI, acute kidney injury; APOL1, apolipoprotein L1; CKD, chronic kidney disease; CKDu, chronic kidney disease of undetermined origin; PKD,

polycystic kidney disease.

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alone and data from the CKD-PC examining the risk of

outcome by GFR stage assessed by eGFRcr compared with

eGFRcr-cys. As compared with equations based on creatinine

and cystatin C alone, the equation using both creatinine and

cystatin C comes closest to mGFR most consistently

(Supplementary Table S3

73–96

). The CKD-PC data were an

individual-level data analysis of 27,503,140 participants

from 114 global cohorts (eGFRcr) and 720,736 participants

from 20 cohorts (eGFRcr-cys) and 9,067,753 participants

from 114 cohorts (albuminuria) from 1980 to 2021 from

around the world conveying a high degree of robustness in

the association of CKD stage with a broad range of adverse

outcomes. Based on the totality and consistenc y of the

CKD-PC data, the overall certainty of the evidence was

rated as moderate.

Values and preferences. This recommendation places a high

value on the need for the most accurate assessment of GFR.

The Work Group judged that many people at risk for CKD

would prefer an accurate measurement when conﬁrming the

diagnosis of CKD and its staging. For this reason, the Work

Group prioritized eGFRcr-cys over eGFRcr or eGFRcys for

the most accurate measurement. The recommendation puts a

low value on the availability and cost of an assessment of

eGFRcr-cys suggesting that people at risk of CKD would opt

for the more accurate assessment.

Resource use and costs. The costs and resource use associ-

ated with eGFRcr-cys are currently greater than those of

eGFRcr; however, the need for an accurate measurement may

offset these expenses. In addition, accurate diagnosis of CKD

as early as possible may lead to lower resource utilization and

healthcare spending than if diagnosed in later stages of CKD.

For more information on the costs assoc iated with cystatin C

assessments, please refer to Section 1.2.2.

Considerations for implementation. The biggest consideration

for implementation is the availability of cystatin C measurement.

For this reason, the recommendation includes the alternative for

eGFRcr in such cases taking into consideration the limitations

and drawbacks of creatinine-based measurements.

Rationale

The KDIGO CKD staging system based on 2 dimensions,

GFR and albuminu ria, was created largely to reﬂect the as-

sociation of outcomes of people with CKD, relative to the

earlier staging systems based solely on GFR stages. Assessment

of GFR stage is ideally performed using accurate assessment

of GFR and ACR and is used to best capture the prognosis for

people with CKD with regard to outcomes such as kidney

failure, CVD, and mortality risk. There is now a large evi-

dence base demonstrating that the use of eGFRcr-cys reclas-

siﬁes a large proportion of the population into different GFR

stages and the “new” stages better reﬂect their risk associa-

tions. For that reason, where available, cystatin C should be

added to creatinine for the purpose of estimating GFR for

CKD diagnosis and staging.

1.1.3 Evaluation of chronicity

Practice Point 1.1.3.1: Proof of chronicity (duration of a

minimum of 3 months) can be established by:

(i) review of past measurements/estimations of GFR;

(ii) review of past measurements of albuminuria or

proteinuria and urine microscopic examinations;

(iii) imaging ﬁndings such as reduced kidney size and

reduction in cortical thickness;

(iv) kidney pathological ﬁndings such as ﬁbrosis and

atrophy;

(v) medical history, especially conditions known to

cause or contribute to CKD;

(vi) repeat measurements within and beyond the 3-

month po int.

Practice Point 1.1.3.2: Do not assume chronicity based

upon a single abnormal level for eGFR and ACR, as the

ﬁnding could be the result of a recent acute kidney injury

(AKI) event or acute kidney disease (AKD).

Practice Point 1.1.3.3: Consider initiation of treatments for

CKD at ﬁrst presentation of decreased GFR or elevated

ACR if CKD is deemed likely due to presence of other

clinical indicators.

Kidney diseases may be acute or chronic.

1,97

We explicitly

yet arbitrarily deﬁne the duration of a minimum of 3 months

(>90 days) as delineating “chronic” kidney disease. The

rationale for deﬁning chronicity is to differentiate CKD

from AKDs (such as acute glomerulonephritis [GN]),

including AKI, which may require different timelines for

initiation of treatments, different interventions, and have

different etiologies and outcomes. The duration of kidney

disease may be documented or inferred based on the

clinical context. For example, a person with decreased GFR

or kidney damage during an acute illness, without prior

documentation of kidney disease, may be inferred to have

AKD. Resolution over days to weeks would conﬁrm the

diagnosis of AKI from a variety of different causes. A

person with similar ﬁndings in the absence of an acute

illness may be inferred to have CKD, and if followed over

time, would be conﬁrmed to have CKD. In both cases,

repeat ascertainment of GFR and kidney damage is

recommended for accurate diagnosis and staging. The

timing of the evaluation depends on clinical judgment, with

earlier evaluation for those suspected of having AKI and

later evaluation for those suspected of having CKD.

For people w ith risk factors for CKD, delaying diag-

nosis for the sake o f conﬁrm ing chronicit y can delay

care. Many people may not recognize the impor tance of

a repeat v isit if treatment had not been initiated. Thus,

initiating treatment both allows for earlier inter vention

and also indicates to people the importance of the

disease.

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Special considerations

Pediatric considerations.

Newborns who clearly have kidney

disease (e.g., severe congenital malformations of the kidney and

urinary tract) do not need to wait 3 months to conﬁrm CKD.

1.1.4 Evaluation of cause

Practice Point 1.1.4.1: Establish the cause of CKD using

clinical context, personal and family history, social and

environmental factors, medications, physical examination,

laboratory measures, imaging, and genetic and pathologic

diagnosis (Figure 8).

Practice Point 1.1.4.2: Use tests to establish a cau se based

on resources available (Table 6

22,98-100

In evaluation of cause, healthcare providers should select

speciﬁc diagnostic tests based on the pretest probability of a

speciﬁc diagnosis informed by clinical presentation. Identiﬁca-

tion of cause confers beneﬁt for targeting therapy to slow pro-

gression to kidney failure, understanding contributing factors,

and prognosis. In addition, identiﬁcation of cause can help

people communicate information about a genetic or familial

cause to relatives, improve understanding of their condition in

the context of self-care management, and improve health literacy.

Genetic testing is emerging as a valuab le component for

evaluation of cause. In some studies, >10% of people with

CKD, regardless of family history, were observed to carr y

genetic pathogenic and likely pathogenic variant(s) that

represent a plausible molecular cause for the development or

progression of CKD.

101–103

In some cases, identiﬁcation of

actionable genes through genetic testing can impact the

clinical management of people with CKD (Figure 9

100

104,105

The prevalence of genetic causes to CKD is expected to

increase in future years through increased recognition.

A recent KDIGO Controversies Conference listed the following

recommendations for when genetic testing can be particularly

informative: (i) high prevalence of monogenic subtypes within the

clinical category , (ii) early age of onset of CKD , (iii) syndromic/

multisystem features, (iv) consanguinity , (v) possibility of iden-

tifying a condition amenable to targeted treatment, and (vi) CKD/

kidney failure of unknown etiology when kidney biopsy would not

be informative due to advanced disease.

100

The KDIGO Controversies Conference also highlighted

the importance of an educated workforce with expertise in

kidney genetics, genomics, and computational research for

appropriate use and interpretation of these tests (Figure

100

). Access to genetic counseling and medical genetics is

important for psychosocial support, appropr iate use of

genetic testing, and to limit costs.

102

Most people with a new diagnosis of CKD and their

healthcare providers would prefer to undertake evaluation for

the underlying cause to ensure that the best possible care is

provided. Althoug h some people identiﬁed as having CKD

may prefer not to undergo the (sometimes invasive) pro-

cedures to evaluate cause, establishing cause enables the most

appropriate management strategy to be implemented.

Resources available for evaluation of cause will vary

worldwide. People may not be able to pay for some diagnostic

tests. Therefore, healthcare providers should tailor the eval-

uation of cause based on these resource constraints (e.g.,

urine protein reagent strip testing instead of ACR).

Education on the value of establishing a diagnosis of CKD

is critical. This can be done through local, national, and in-

ternational kidney societies and within healthcare training

programs (Chapter 5). Additional resources may be required

to support wider scale implementation of diagnostic tests,

especially genetic testing, availability of biopsies, and the

support required for implementation.

Identiﬁcation of cause is often achieved by standard clin-

ical methods (i.e., history and examinat ion), knowledge of the

causes of CKD and their manifestations (i.e., level of GFR and

speciﬁc marker of kidney damage such as hematuria, urine

albumin, or cysts), together with specialized investigations

(Figure 8). Not all evaluations of cause are required in all

people. Information from the clinical context and initial

tests may lead to further evaluatio ns ( Table 6), which are

likely to be conducted as part of specialized kidney care

services and dependent on resources (Chapter 5).

Recommendation 1.1.4.1: We suggest performing a

kidney biopsy as an acceptable, safe, diagnostic test

to evalu ate cause and guide treatment decisions

when clinically appropriate (2D).

This recommendation places a high value on an acceptable safety

proﬁle of kidney biopsies when used to evaluate the cause of

CKD and to plan appropriate treatment.

Key information

Balance of bene ﬁts and harms.

The beneﬁts of kidney bi-

opsy in terms of diagnosis, prognosis, and planning appro-

priate treatment for both the person with CKD and healthcare

Physical

exam

Nephrotoxic

medications

Symptoms and signs

of urinary tract

abnormalities

Symptoms and signs

of systemic diseases

Laboratory tests, imaging, and tissue sample, such as:

• Urinalysis and urine sediment

• Urine albumin-to-creatinine ratio

• Serologic tests

• Ultrasound

• Kidney biopsy

• Genetic testing

Medical

history

Social and

environmental

history

Obtain careful family history

for possible genetic causes,

including family pedigree for CKD

Figure 8 | Evaluation of cause of chronic kidney disease (CKD).

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providers are through improved understanding of the iden-

tiﬁed disease state and the extent of active and chronic lesions.

The harms include the possibility of complications of the

procedure (bleeding risk/pain), the obtaining of a non-

diagnostic or insufﬁcient sample (wasted resource), and the

anxiety induced while awaiting the results.

The systematic review performed by the ERT identiﬁed 37

studies assessing the prognostic beneﬁ t and safety of kidney

biopsy among people with CKD. Ten studies examined the

diagnostic and/or prognostic beneﬁt of kidney biopsy or in-

ﬂuence of biopsy results on management decisions. The

diagnostic ﬁndings were heterogeneous and variable, which

did not lend themselves to further synthesis. The rate of

mortality after native kidney biopsy in people with suspected

or diagnosed CKD was low. Across the 15 studies that re-

ported on mortality after a native kidney biopsy, there were 3

reported deaths. The rate of perirenal hematoma across 14

studies was estimated to be 16% (95% conﬁdence interval

[CI]: 12%–22%). No studies reported on retroperitoneal

hemorrhage (Supplementary Table S4

106–126

Certainty of evidence. The overall certainty of evidence for

kidney biopsy andoutcomes of harms is very low (Supplementary

Table S4

106–126

). The critical outcomes, mortality and perirenal

hematomas, were primarily assessed in observational studies

without a comparison group. Because of the potential for

confounding, the ERT cons ider ed the body of evidence to have

Table 6 | Guidance for the selection of additional tests for evaluation of cause

Test category Examples Comment or key references

Imaging Ultrasound, intravenous urography, CT kidneys

ureters bladder, nuclear medicine studies, MRI

Assess kidney structure (i.e., kidney shape, size, symmetry, and evidence of

obstruction) for cystic disease and reﬂux disease.

Evolving role of additional technologies (e.g., 3D ultrasound)

Kidney biopsy Ultrasound-guided percutaneous Usually examined by light microscopy, immunoﬂuorescence, and electron

microscopy, and, in some situations, may include molecular diagnostics

Used for exact diagnosis, planning treatment, assessing activity and

chronicity of disease, and likelihood of treatment response; may also be

used to assess genetic disease

Laboratory tests:

serologic, urine

tests

Chemistry including acid-base and electrolytes,

serologic tests such as anti-PLA2R, ANCA, anti-GBM

antibodies

Serum-free light chains, serum, and urine protein

electrophoresis/immunoﬁxation

Urinalysis and urine sediment examination

Refer to KDIGO 2021 Clinical Practice Guideline for the Management of

Glomerular Diseases

Increasing recognition of the role of light chains in kidney disease even in

the absence of multiple myeloma (monoclonal gammopathy of renal

signiﬁcance [MGRS])

Presence of persistent hematuria or albuminuria is critical in determining

differential diagnosis

Genetic testing APOL1, COL4A3, COL4A4, COL4A5, NPHS1, UMOD,

HNF1B, PKD1, PKD2

Evolving as a tool for diagnosis, increased utilization is expected.

Recognition that genetic causes are more common and may present

without classic family history

99,100

ANCA, antineutrophil cytoplasmic antibody; APOL1, apolipoprotein 1; COL4A, type IV collagen alpha chain; CT, computed tomography; GBM, glomerular basement membrane;

HNF1B, hepatocyte nuclear factor 1B; MRI, magnetic resonance imaging; NPHS1, congenital nephrotic syndrome; PKD1, polycystic kidney disease-1; PKD2, polycystic kidney

disease-2; PLA2R, M-type phospholipase A2 receptor; UMOD, uromodulin.

Conditions amenable

to specific disease-

modifying therapies

Avoidance of

prolonged

immunosuppressive

therapies

Conditions at risk for

recurrence after

kidney transplantation

Conditions for which

genetic testing is

relevant for reproductive

counseling

Examples:

• GLA (Fabry)

• AGXT (primary

hyperoxaluria (PH))

• CoQ10 genes (SRNS)

• CTNS (cystinosis)

• Tubulopathies

(Na

, K

etc.)

Conditions amenable

to nonspecific

renoprotective

strategies

Example:

• COL4A3/4/5 (Alport)

and RAAS blockade

Example:

• Glomerular disease

due to mutations in

Alport genes

(COL4A3/4/5)

Examples:

• (CFH/CFI/C3...): aHUS

• (AGXT, GRHPR,

HOGA): primary

hyperoxaluria (PH)

• Adenine phosphoribo-

syltransferase deficiency

(APRT)

Conditions amenable

to specific screening

for extrarenal

manifestations

Examples:

• HNF1B: diabetes

• PKD1/PKD2

(ADPKD): intracranial

aneurysms

• FLCN: renal cell

carcinoma, etc.

Example:

• Prenatal/preimplantation

diagnosis

Figure 9 | Actionable genes in kidney disease. Actionability refers to the potential for genetic rest results to lead to speciﬁc clinical actions

from prevention or treatment of a condition, supported by recommendations based on evidence. ADPKD, autosomal dominant polycystic

kidney disease; aHUS, atypical hemolytic uremic syndrome, CKD, chronic kidney disease; RAAS, renin-angiotensin-aldosterone system, SRNS,

steroid-resistant nephrotic syndrome. Reproduced from KDIGO Conference Participants. Genetics in chronic kidney disease: conclusions from a

Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2022;101:1126–1141.

100

Disease: Improving Global Outcomes (KDIGO). Published by Elsevier Inc. on behalf of the International Society of Nephrology. This is an open

access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

chapter 1 www.kidney-international.org

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Kidney International (2024) 105 (Suppl 4S), S117–S314

serious study limitations. The certainty of the evidence for

mortality was further downgraded because there were few

events reported. The certainty of the evidence for perirenal

hematomas was downgraded because there was signiﬁcant

statistical heterogeneity in the results across studies. The ERT

did not identify any studies that reported on the critical

outcome of retroperitoneal hemorrhage.

Values and preferences. The Work Group judged that many

people with CKD would choose to undergo a kidney biopsy

to establish the cause of their CKD more accurately and

potentially offer prognostic information. Thus, this recom-

mendation puts a high value on the speciﬁcity of a kidney

biopsy for the evaluation of cause as well as the very low

certainty evidence demonstrating a low risk of complications

associated with kidney biopsy. Because the potential that the

information gleaned from the biopsy may not directly or

immediately beneﬁt the person, the Work Group jud ged that

some people may prefer to decline a kidney biopsy. The de-

cision to pursue biopsy should be a shared decision and be

informed by probability of and utility of the information

obtained on both diagnostic and prognostic fronts.

Resource use and costs. Resources available for evaluation

of cause w ill vary worldwide and is dependent on the

healthcare systems. People with CKD may not be able to pay

for biopsy or afford the time away from work for the pro-

cedure. Resources in speciﬁc countries may not permit

appropriate analysis of the obtained samples. Thus, healthcare

providers’ decisions to perform a kidney biopsy in the pres-

ence of limited resources may therefore be inﬂuenced based

on expected yield for that individual and the perceived value

of the extra information gained.

Considerations for implementation. To optimize beneﬁt and

safety, a standardized approach for kidney biopsy with a

vetted and standardized operating protocol designed for local

implementation is warranted. Of note, most studies reported

using ultrasound-guided biopsies and older literature sug-

gesting higher bleeding rates were conducted in the absence

of guided biopsies; thus, we might infer that there is a po-

tential for higher rate of harms in “blind”/unguided biopsies.

Rationale

Kidney biopsy is an important par t of the investigations for

the cause of CKD. It is often deferred because of the potential

for harm or lack of recognition of potential utility. The evi-

dence to support safety of biopsy is heterogeneous and

therefore uncertain, but in the studies evaluated, appears to

confer low risk of harm, supporting our suggestion that

kidney biopsies should be considered when it is thought that

they can provide information to identify cause, facilitate

prognostication, and inform treatment strategies.

Special considerations

Pediatric considerations.

Children and young people with

kidney failure are more likely to have a genetic cause of their

disease than adults. In so me healthcare settings, genetic

testing may be pursued ﬁrst, obviating the need for kidney

biopsy and the associated risks, which may be different in

children than adults.

1.2 Evaluation of GFR

The kidney has many functions, including excretory, endo-

crine, and metabolic functions. GFR is one component of

Centers of expertise

(multidisciplinary teams)

All nephrology

clinics

Connections with geneticists

and genetic counselors

Number of nephrologistsClinic type Knowledge level

High

Medium

Basic

As many

as possible

Few

All

Source of knowledge

Advanced training and

subspecialties and extensive

clinical experience

CME courses, workshops

and heuristically based

Medical school/

fellowships/licensing

Figure 10 | Proposed organization for implementing genetics in nephrology. Within a health system, multiple center types, provider

specialties, and education strategies are needed for optimal implementation of genetics in nephrology. A 3-tiered organization model includes

the following: (i) a basic, common level of knowledge in genetics among all nephrologists; (ii) clinical connections between nephrologists and

geneticists and genetic counselors; and (iii) centers of expertise where nephrologists with genetic expertise collaborate with geneticists and

genetic counselors. CME, continuing medical education. Reproduced from KDIGO Conference Participants. Genetics in chronic kidney disease:

conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2022;101:1126–1141.

100

Copyright ª 2022, Kidney Disease: Improving Global Outcomes (KDIGO). Published by Elsevier Inc. on behalf of the International Society of

Nephrology. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Kidney International (2024) 105 (Suppl 4S), S117–S314 S175

excretory function but is widely accepted as the best overall

index of kidney function because it is generally reduced after

widespread structural damag e and most other kidney func-

tions decline in parallel with GFR in CKD.

In this section, we describe the overall approach for the

evaluation of GFR. As in the previous KDIGO Clinical

Practice Guideline for the Evaluation and Management of

Chronic Kidney Disease,

the ﬁrst method to evaluate GFR

should be eGFRcr. If necessary for greater accuracy, the

approach then recommends subsequent supportive tests

from either the more accurate eGFRcr-cys or measurement

of GFR using urinary or plasma clearance of exogenous

ﬁltration markers. In contrast to the previous guideline, we

emphasize the use of eGFRc r-cys based on accumulating

evidence for its greater accuracy across populations and the

use of mGFR given the known residual errors in all

estimating equations. We also describe laboratory

techniques and standards that satisfy the requirements for

robust result reporting. We encourage healthcare providers

to have a clear understanding of the value and limitations

of both ﬁltration markers and mGFR, the importance of

standardization of assays for creatinine and cystatin C, and

quality control procedures for exogenous markers. Finally,

we describe cur rently available, validated estimating

equations that can be used for the reporting of GFR by

clinical laboratories.

1.2.1 Other functions of kidneys besides GFR

Practice Point 1.2.1.1: Use the term “GFR” when referring

to the speciﬁc kidney function of glom erular ﬁ ltration. Use

the more general term “kidney function(s)” when dealing

with the totality of functions of the kidney.

The kidneys play several roles in the body, including

metabolism and excretion of substances, volume and BP

regulation, er ythropoietin production, and regulation of

electrolytes, acid-base status, and mineral homeostasis.

Glomerular ﬁltration is one of many functions of the kidney.

GFR is considered the best overall assessment of kidney

functions as, in general, losses of these other functions

correlate with the loss of GFR. The term “kidney function”

reﬂects the entirety of different and complex physiological

functions of the kidney ; thus, kidney function should not be a

term used interchangeably with GFR.

Assessment of the overall functions of the kidney is a

complex task. GFR is used as the primary tool to assess kidney

function in practice. Loss of other kidney functions are

known as complications of CKD and are addressed in

Chapter 3. This section focuses on how GFR can be evaluated

using both mGFR and eGFR.

Special considerations

Pediatric considerations.

There are numerous kidney dis-

orders in children that may present with tubular dysfunction

(e.g., Bartter’s and Dent disease) rather than decreased GFR

or albuminuria. These pr imarily result in polyuria and/or

electrolyte disturbances and may or may not progress to

reduced GFR or kidney failure. Thus, the exclusive use of GFR

in diagnosing CKD would not be of value in children, high-

lighting the importance of appreciating different markers

linked to different kidney functions.

1.2.2 Guidance to physicians and other healthcare providers

We describe a framework for evaluation of GFR beginning

with an initial test and followed by additional supportive tests

(Figure 11, Tables 7 and 8

127–142

Figure 11 depicts an algorithm for evaluation of GFR from

initial test using eGFRcr, followed by decisions for when to

perform supportive tests such as cystatin C or mGFR

(Tables 7 and 8). Healthcare prov iders should consider both

potential sources of error in eGFR as well as whether the

clinical decision requires a highly accurate GFR when

considering the need for additional tests. The level of

accuracy that is needed for a clinical decision for the use of

potentially toxic medications, a medication with a narrow

therapeutic window, or for other therapies with potential

for adverse events, may exceed the capability of any eGFR

equation, and in such cases, mGFR should be performed.

This assessment would ideally be performed every time a

GFR value is used to make a clinical decision.

Practice Point 1.2.2.1: Use serum creatinine (SCr) and

an estimating equation for initial assessment of GFR

(Figure 11).

There are no RCTs to quantify the impact for the use of

less accurate methods versus more accurate methods of

assessment of GFR. For most clinical circumstances, esti-

mating GFR from SCr is appropriate for diag nosis, stagin g,

and monitoring the progression of CKD, and observational

data documented an increase in CKD recognition and referral

to nephrologists shortly after the implementation of reporting

of eGFR by clinical laborator ies, especially for females and

elderly people.

143–145

GFR is used in many routine and

complex clinical decisions as an assessment of excretory

kidney function (Table 4) to detect and stage AKD and CKD,

determine CKD progression, dose medications, determine

appropriate use of diagnostic tests, and guide treatment

decisions around KRT therapies. Equations are available

that estim ate GFR using SCr and adjusting for sex and age,

and professional societies throughout the world have

recommended that GFR estimates should be used in

association with SCr reporting . Sources of error in GFR

estimation from SCr concentration include non–steady-state

conditions, non-GFR determinants of SCr, measurement

error at higher GFR, and interferences with the creatinine

assays. GFR estimates are less precise at higher GFR levels

than at lower levels, and healthcare providers should remain

aware of caveats for any estimating equation that may

inﬂuence the accuracy in an individual person.

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Most people with CKD and their healthcare pr oviders would

prefer the more accurate assessment of kidney function resulting

from the use of GFR estimating equations compared with SCr

alone. Minimal cost or resources issues are expected because

creatinine is available in healthcare settings globally, and evalu-

ating GFR with the use of creatinine in the form of GFR esti-

mating equations has been recommended for >20 years.

eGFR from creatinine is widely used. Attention is required

to implement and ensure the quality of eGFR reporting by

clinical laboratories and ensure coordination with the elec-

tronic medical record (EMR), including those eGFR reports

from point-of-care settings (Section 1.2.2).

Recommendation 1.2.2.1: We recommend using

eGFRcr-cys in clinical situations whe n eGFRcr is less

accurate and GFR affects clinical decision-making

(Table 8

127-142

) (1C).

This recommen dation places a high value on using estimates of

GFR derived from a combination of creatinine and cystatin C in

clinical situations where eGFRcr is an unreliable or inadequate

assessment of GFR. There is consistent evidence that eGFRcr-cys

provides more accurate estimates of mGFR than eGFRcr and

eGFRcys in ambulator y people.